Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study of liver abnormalities in 36 patients with mixed cryoglobulinemia in the absence of underlying infectious, connective tissue, or lymphoproliferative disorders revealed clinical or biochemical evidence of liver dysfunction in 84%. Hepatomegaly was detected in 77%, splenomegaly in 54%, and abnormalities in bilirubin, alkaline phosphatase, or serum glutamic oxalacetic transaminase in 77%. Only four of the patients had overt liver disease. Of 15 biopsies from 12 patients, there was normal tissue structure in two, minimal nonspecific changes in one, portal fibrosis in three, chronic persistent hepatitis in one, chronic active hepatitis in two, chronic active hepatitis with cirrhosis in four, and postnecrotic cirrhosis in two. These findings, together with the previously reported high incidence of serologic evidence of hepatitis B virus (HBV) infection, support the view that the syndrome of purpura, arthritis, and nephritis is often a consequence of immune-complex vasculitis secondary to HBV infection.
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PMID:Liver involvement in the syndrome of mixed cryoglobulinemia. 90 Jun 72

This study was designed to compare the clinical and immunological characteristics of the hepatitis B surface antigen (HBsAg)-positive and HBsAg-negative (cryptogenic) forms of chronic active hepatitis. The data of 48 patients with chronic active hepatitis, 24 with persistent HBs antigenemia and 24 without HBsAg, were analysed. HBsAg was detected by counter-immunoelectrophoresis and radioimmunoassay. The clinical features, biochemical liver function tests, immunoglobulins, complement C3, antoantibodies, and cell-mediated immunoreactivity of the two forms of the disease were compared. Cirrhosis was found to occur more frequently at the time of diagnosis in the HBsAg-negative group, and the serum alkaline phosphatase level was raised significantly compared to the HBsAg-positive form. The elevation of the IgG level was greater in the cryptogenic form, but the difference was not statistically significant compared to the HBsAg-positive patients. There was a marked difference in the frequency of the mitochondrial antibodies, but not of the antinuclear factor and other autoantibody-like serum factors. Lymphoblastic transformation revealed a similar diminution in response to phytohaemagglutinin stimulation in both groups of patients compared to the normal controls. An increase of the 3H-thymidine incorporation was seen after stimulation with human liver mitochondrial antigen, and leukocyte migration inhibition could be observed with this antigen in both forms of chronic active hepatitis.
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PMID:Chronic active hepatitis in patients with and without hepatitis B surface antigenemia. 91 64

Four patients with chronic hepatitis B infection and chronic active hepatitis were treated with human leukocyte interferon. Three of them had consistently elevated levels of circulating Dane-particle markers, including Dane-particle-associated DNA polymerase activity, hepatitis B core antigen and Dane-particle-associated DNA. Parenteral interferon administration at a dosage between 6.0 X 10(3) and 17 X 10(4) U per kilogram per day was associated with a rapid and reproducible fall in all Dane-particle markers in the three patients. The suppressive effect was transient when the interferon was given for 10 days or less but appeared to be more permanent when administration was prolonged for a month or more. In addition, long-term interferon therapy was associated with a marked fall in hepatitis B surface antigen in two of three patients and a disappearance of e antigen in two of two patients. Interferon may be useful in limiting carrier infectivity or eradicating chronic infection.
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PMID:Effect of human leukocyte interferon on hepatitis B virus infection in patients with chronic active hepatitis. 95 Sep 57

To document the sequelae of acute hepatitis among recipients of commercial and volunteer blood and to assess factors influencing the development of chronic hepatitis (CH), 47 patients with post-transfusion hepatitis were followed prospectively from the time they received their transfusions. Twenty-nine had prolongation of at least 2-fold serum glutamic pyruvic transaminase (T) elevations for more than 20 weeks, and were classified as CH. When the patients with CH were compared to those with only acute hepatitis (abnormal T for less that 20 weeks), no difference was found with respect to age, sex, number of units transfused, incubation period, presence or absence of symptoms, occurrence of jaundice, maximum T, receipt or development of hepatitis B surface antigen or antibody, underlying illness, or area of the hospital where the patient was treated. Liver biopsies in 15 of the 29 revealed chronic-active hepatitis in 9, chronic persistent hepatitis in 2, unresolved hepatitis in 4. Five of the 9 patients with chronic active hepatitis were without symptoms. None of these died or have developed cirrhosis. Because chronic liver disease frequently developed after acute post-transfusion hepatitis among multiply transfused hepatitis B surface antigen negative blood recipients, close follow-up, including liver biopsy, is warranted in such patients with prolonged transaminase elevations.
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PMID:Post-transfusion chronic liver disease. 96 71

Sera of 103 carriers of hepatitis B surface antigen were assayed for e-antigen and anti-e. Twenty-four were e-antigen-positive, 31 anti-e-positive, and 48 had neither detectable (e-negative). Aminotransferases were elevated in 75% of the e-antigen-positive carriers compared with 25% of e-negative carriers (P less than 0.001) and 13% of anti-e-positive carriers (P less than 0.001). Serum DNA polymerase activity was significantly higher in the e-antigen-positive carriers than in carriers without e-antigen. Dane particles were shown in 10 of 12 carriers with e-antigen, compared with one of 12 e-negative carriers (P less than 0.0003) and none of 12 anti-e-positive carriers (P less than 0.00003). These results suggest that ongoing hepatitis B viral replication is more active in e-antigen-positive carriers than in carriers without e-antigen, a finding that may help explain the high prevalence of chronic active hepatitis described in these individuals.
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PMID:"e" Antigen, Dane particles, and serum DNA polymerase activity in HBsAg carriers. 97 Jul 72

Cell-mediated immunity (CMI) to hepatitis B surface antigen (HBsAg) was investigated in patients who recovered from acute hepatitis B and in chronic carriers of the antigen, either with or without liver disease. The study was performed using leucocyte migration inhibition test and purified HBsAg. In antigen-negative post-hepatitis patients the frequency of cellular immunity to HBsAg (63.6%) showed a significant difference to controls. On the other hand, only one out of 5 antigen-positive post-hepatitis patients showed sensitisation to HBsAg; four out of these cases had chronic hepatitis at liver biopsy. In HBsAg-chronic carriers, with or without liver disease, the frequency of CMI to HBsAg was not significant to controls. A significant correlation was noted between inflammatory activity and inhibition of migration. Our results suggest that a normal cellular immune response to HBsAg is necessary for the recovery from acute hepatitis B and for the clearance of the virus. In HBsAg-chronic carriers this response seems to be absent or inadequate, leading to the state of healthy chronic carriers or to the evolution to HBsAg-chronic hepatitis, respectively. The high frequency of CMI in HBsAg-negative chronic active hepatitis, suggests that hepatitis B virus infection may play a role in the ethiology of the disease.
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PMID:[Infection due to hepatitis B virus and host immune response]. 101 86

Cell-mediated immunity to a liver specific membrane protein (LP1) has been studied in patients with different types of liver diseases, using the leucocyte migration inhibition test. A high frequency of cellular sensitization to LP1 was detected in untreated chronic active hepatitis, with no significant differences between HBsAg-positive and negative cases. Inhibition of migration is a long-lasting reaction in the spontaneous evolution of the disease, while immunosuppressive treatment normalizes the test only in cases with complete remission. In viral hepatitis B cell-mediated immunity to the liver specific membrane protein can be detected in the acute phase of the disease as a time-limited reaction, exhausted with the clearance of the virus from the liver. An inhibition of migration with LP1 was found also in some cases of HBsAg-positive post-hepatitis patients, in chronic persistant hepatitis, mainly HBsAg-positive, and in asymptomatic chronic carriers of the antigen B. Most of these cases showed a progression to chronic active hepatitis, in clinical and histopathological prospective studies. Our results suggest that cell-mediated immune response to liver specific antigens plays a major role in the pathogenesis of chronic active hepatitis. Moreover the evaluation of these reactions in chronic liver diseases may help in the diagnosis and in the control of the immunosuppressive therapy. Hepatitis B virus infection must be considered one of the possible cause responsible for the rising of autoimmunity to the liver.
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PMID:[Liver-specific proteins and autoimmunity in inflammatory liver diseases]. 101 92

A role has recently been assigned to cell-mediated immunity in chronic liver diseases in addition to the well-known alterations of humoral immunity. We now report the results of the rosette inhibition test for the evaluation of T-lymphocyte "sensitization" in patients with different chronic liver disorders. A cell-mediated immune reaction was found in 81% of patients with chronic active hepatitis and in 71% with primary biliary cirrhosis, whereas patients with chronic persistent hepatitis showed no reaction. The correlation with the incidence of hepatitis B antigen showed that T-lymphocyte sensitization was more frequent in the group of HB-positive patients. Finally, improvement of the test was observed in four out of nine patients given immunosuppressive treatment.
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PMID:Rosette inhibition test in chronic liver disease. 108 10

Serum antibodies to double-stranded 'native' DNA have been measured in acute and chronic liver diseases using the Farr technique. Elevated levels of DNA binding were found in all groups of patients, with the highest levels in acute viral hepatitis and lowest in primary biliary cirrhosis. All patients with hepatitis B surface antigen-positive chronic active hepatitis had elevated levels, hence persistent elevation of DNA binding after acute type B hepatitis might be an unfavourable prognostic marker indicating progression to chronic active hepatitis, DNA antibody levels will not offer diagnostic help in liver diseases, or help to follow the response of patients with 'lupoid' hepatitis to corticosteroid therapy. Production of DNA antibody may be a response to release of DNA from damaged hepatocytes.
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PMID:Double-stranded DNA-binding capacity of serum in acute and chronic liver disease. 108 14

This study concerns hepatitis B antigen and antibody, (HBAg and HBAb) auto-antibodies and liver disease in a renal haemodialysis and transplantation unit between February, 1970 and December, 1972. Fourteen per cent of patients on maintenance haemodialysis, 25% of renal transplant recipients, and 5% of the staff were HBAg positive during this period. Three family members of antigen positive patients developed hepatitis; all were either antigen or antibody positive. Both immuno-electro-osmo-phoresis and radio-immuno-assay were used to detect HBAg. No additional carriers were identified among the dialysis or transplant patients by applying the more sensitive technique, although two persons with hepatitis were positive only by RIA. None of the staff members who developed antigen positive hepatitis died, and no one became a carrier. Dialysis patients who had icteric hepatis also cleared the antigen from the serum. Clinical hepatitis did not occur in immunosuppressed graft recipients who were carriers of the ay subtype of the antigen, nor was there histological evidence of liver disease in 18 of 19 of such carriers studied. Moreover, there was no association between long term carriage of the antigen and the presence of the auto-antibodies characteristic of chronic active hepatitis. Rapid reduction of immunosuppression was followed by acute hepatitis in one carrier, while another, whose antigen was of the ad subtype, developed micro-nodular cirrhosis.
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PMID:Hepatitis B antigen, auto-antibodies and liver disease in a haemodialysis and transplantation unit. 110 68


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