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)

Four patients who had chronic liver disease and were positive for hepatitis B surface antigen (HBsAg) were treated with vidarabine, a synthetic purine nucleoside that inhibits DNA polymerase activity in vitro and in vivo. Before treatment all had raised serum DNA polymerase concentrations. Three also had hepatitis B e (HBe) and were shown by electron microscopy to have hepatitis B virus (Dane) particles in their serum. In all patients 10 days' treatment with vidarabine resulted in an immediate loss of DNA polymerase activity. In three patients the activity returned when treatment was stopped. In those three patients Dane particles and HBe antigen persisted during and after treatment; in the fourth patient, who remained negative for DNA polymerase, HBsAg titres fell. Although vidarabine inhibited virus replication, virus particles did not disappear from the blood in these patients, presumably because the particles were cleared only slowly. Similar results with interferon suggest that the virus disappears, and HBsAg titres fall, some weeks after the fall in DNA polymerase activity. Continued treatment may therefore have a sustained effect on viral replication. Whether vidarabine can permanently clear HBsAg and so arrest chronic liver disease remains to be seen, but at the very least it could reduce the spread of infection.
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PMID:HBsAg-positive chronic liver disease: inhibition of DNA polymerase activity by vidarabine. 69 57

Circulating complete and defective hepatitis B virus forms, as represented by full, DNA polymerase-positive and empty, DNA polymerase-negative Dane particles, respectively, were investigated in sera from patients with chronic hepatitis B virus infection and related to the presence of e antigen and antibody and to the histological findings on liver biopsy. Complete hepatitis B virus particles were detected in the serum of all patients postive for e antigen, their percentage ranging from 15 to 61% of the total Dane particle population. Although most of these cases had chronic persistent or chronic active hepatitis, complete viral particles were also found in serum of 3 healthy carriers of hepatitis B surface antigen who had e antigen. These results indicate that e antigen is a marker of active virus replication and support its association with infectivity. It is also associated with liver damage because production of complete virus is a feature of chronic hepatitis. In the presence of anti-e, detection of Dane particles in serum appeared to be related to the histological findings. Most of the healthy carriers had no Dane particles in serum, whereas 80% of the cases with chronic liver disease had circulating Dane particles. However, in contrast to the cases with e antigen, 98 to 100% of Dane particles in these cases appeared to be defective in nucleic acid material on electron microscopy after positive staining. All of the patients with chronic active hepatitis in this group had progressed to cirrhosis and it is possible that production of complete virus particles is reduced in the later stages of the illness.
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PMID:Full and empty Dane particles in chronic hepatitis B virus infection: relation to hepatitis B e antigen and presence of liver damage. 70 Mar 29

The in vitro correlates of cell-mediated immunity to liver tissue antigens and hepatitis B surface antigen (HBsAg) were studied in groups of subjects with acute and chronic hepatitis B virus (HBV) infection and in a population of HBV-seronegative controls. The technique of in vitro lymphocyte transformation (LTF) was employed in these studies. No LTF response to liver-specific antigen and HBsAg was observed in the control population. LTF activity in response to HBsAg was present in 11 of the 14 subjects with acute type B viral hepatitis during the early phase of the disease, and eight of these subjects also had LTF reactivity to liver antigen. During the convalescent phase the LTF reactivity to these antigens usually disappeared. More than 70% of patients with chronic carriage of HBsAg who had elevated levels of liver enzymes showed LTF responses to HBsAg, and a significant number of these subjects also exhibited LTF response to liver-specific antigen. On the other hand, chronic HBsAg carriers who persistently showed normal liver enzyme values (asymptomatic carriers) failed to show significant responses to liver antigen or HBsAg. It is suggested that the persistence of cellular reactivity to liver antigens may lead to the establishment of chronic liver disease.
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PMID:Cell-mediated immune response to liver tissue antigen and hepatitis B surface antigen after infection with hepatitis B virus in humans. 71 16

To assess the hepatitis B virus infection risk to household contacts exposed to HBsAg-positive chronic carriers, 169 family members of 20 healthy carriers of HBsAg and of 12 with chronic hepatitis were followed up prospectively for two to five years. All family members are investigated for the presence of serum HBsAg/antiHBs system and for the presence of liver disease. Our results indicate that the family contacts of HBsAg carriers with evidence of chronic liver disease are at greater risk of exposure to HBV than the contacts of healthy carriers and that acquisition of HBsAg is more common among males than among females. Evidence of exposure to HBsAg is very frequent in young age with a striking rise between 10 and 20 years. On the contrary acquisition of anti-HBsAg is more common after 40 years of age. These data suggest that persistent circulation of HBV in a family of chronic HBsAg carrier increases the risk of infection in household contacts and that HBV is eliminated in a more infective form from the carriers with chronic liver disease.
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PMID:[Role of chronic HBsAg carriers in intrafamilial diffusion of hepatitis B virus infection]. 72 68

The probable etiology and outcome of bridging hepatic necrosis found on a liver biopsy performed within three months of the onset of clinical illness was evaluated in 42 consecutive patients with this finding. Eighteen of the patients (43%) had a probable drug etiology for their hepatitis. Ten patients had HBSAG-positive acute hepatitis. Fourteen patients had neither drug-induced disease nor proven HBSAg-positive hepatitis. One patient from the drug-induced group died, but the other 17 had complete clinical recovery. Eight of ten in the hepatitis B antigen-postive group cleared their antigen and had complete clinical recovery. Chronic hepatitis developed in two who remained persistently HGSAg positive. Eight of the patients in the group with unknown etiology recovered, while six developed evidence of active chronic liver disease. This incidence of active chronic liver disease is significantly greater than that found in the drug-induced group (P less than 0.02). We conclude that drug-induced hepatitiis accounts for a significant proportion of patients of acute hepatitis who have bridging hepatic necrosis on liver biopsy. However, in these drug-induced cases the finding of bridging hepatic necrosis does not appear to be associated with an increased risk of development of active chronic liver disease.
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PMID:Bridging hepatic necrosis. Etiology and prognosis. 73 15

329 patients with acute ouvert viral hepatitis which occurred in the Hannover area 1975 were classified according to virological data. The proportions of type A and type non A - non B hepatitis were each approximately 20 percent of the total cases (n = 60). Viral hepatitis B was the most frequent type of viral hepatitis (n = 209). 174 individuals of the 329 hepatitis patients were reexamined serologically two years after the onset of the acute disease. 7 out of 105 patients with hepatitis B (6,7%) and 5 out of 40 patients with hepatitis non A - non B (12,5%) revealed a serological pattern compatible with chronic hepatitis. In contrast none of 29 patients with hepatitis A indicated chronic liver disease. The frequency of anti-HAV was also determined in 41 patients with HBsAg positive and HBsAg negative histologically proven chronic hepatitis or liver cirrhosis. All patients were under 35 years of age. An equal proportion of anti-HAV was found in both groups. These results suggest that hepatitis A practically never results in chronic hepatitis, while hepatitis non A - non B can run a chronic course with a frequency similar to that of hepatitis B.
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PMID:[Chronic hepatitis as sequela of acute viral hepatitis A and hepatitis non A - non B (author's transl)]. 74 46

The clinical course is reported in 17 patients in whom the histological picture of subacute hepatic necrosis ("bridging hepatitis") was found on needle liver biopsy or at autopsy. The patients' ages ranged from 10-71 years, 12 patients being less than 40 years old. Ten patients were males. Jaundice lasted 2-4 months in nine cases and over six months in two, one of the latter having developed cirrhosis. In five patients a relapse of jaundice occurred within three months. Hepatitis B antigen was found in one of 13 patients tested. Two patients died in fulminant hepatic failure, one developed cirrhosis. These three patients and an additional two received prednisone therapy. Twelve of the remaining patients were followed for periods of 8-81 months; an additional two patients' follow-up was incomplete. None developed clinical evidence of chronic liver disease, and laboratory data at the last examination were normal except for slight elevation of alkaline phosphatase in six cases. Repeat biopsies showed persistent hepatitis in one case, slight portal fibrosis in one, cirrhosis in one and at autopsy in a patient who died of unrelated causes two years after hepatitis no evidence of chronic liver disease was found. This relatively good outome of subacute hepatic necrosis is probably due to the young average age of the patients, and the low incidence of B hepatitis in this series.
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PMID:The clinical course of subacute hepatic necrosis. 74 11

Since morbidity of viral hepatitis B is increasing, the causes of diffusion of this infection have been studied. There are several routes of transmission and undoubtedly apparent non-parenteral routes have a great importance. In a study performed on 32 families of HBsAg carriers, familial aggregation of infection has been acquired through close personal contact. Transmission of infection from mother to infant may occur transplacentally for vertical transmission, or, after the birth, for horizontal transmission, so that a high percentage of children is infected. Percutaneous transmission of hepatitis B in families affected by scabies is evident. The presence of infectivity markers is of major importance for transmission of virus: these are HBeAg and specific DNA-polymerase activity of serum. Well, when the carrier exhibits the markers, the contacts are involved in the infection in a high percentage. From this point of view the carriers with chronic liver disease are more dangerous than the asymptomatic ones. The problem of carrier exists: nevertheless it is possible to carry out a better prophylaxis, if we take into account the presence of the infectivity markers.
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PMID:[Factors of contagiousness in the epidemiology of hepatitis type B (author's transl)]. 75 49

Although blood banks in this country have been testing every unit of blood for hepatitis B surface antigen (HBSAg) by one of the highly sensitive "third generation" methods (radioimmunoassay or reversed passive hemagglutination) since September, 1975, post-transfusion hepatitis (PTH) still remains the major hazard to patients who require transfusion with blood and blood products. Since there may be an interval of many months between transfusion and onset of PTH and many cases are subclinical, the best data on the incidence of PTH have come from prospective studies with careful follow-up of transfused patients. Such studies first established the validity of HBSAg as a marker for the presence of hepatitis B virus (HBV), and they have shown a dramatic reduction in the incidence of post-transfusion type B hepatitis following the elemination of HBSAg positive blood from transfusion. Nevertheless, PTH cases not associated with HBV or HAV, which are termed non-A, non-B hepatitis, continue to occur commonly among transfused patients. Non-A, non-B hepatitis appears to be subclinical in many instances, but it can produce prolonged persistence of abnormal liver function tests, which may be associated with chronic liver disease. The outstanding risk factor responsible for the development of PTH has been shown to be blood from paid donors in every study which has evaluated this factor. HBSAg and anti-HBS prevalences were found to be much higher in paid donor groups than in voluntary donors. Accordingly, the Food and Drug Administration has proposed that all units of blood be labeled to indicate whether they were collected from voluntary or paid donors in order to inform consumers of the relative hepatitis risks of blood units from these different donor populations. In addition to HBSAg testing and reduced use of blood from paid donors, measures which may provide future reduction of the hepatitis hazard associated with blood transfusion include avoidance of unnecessary transfusions, identification of the agent(s) responsible for non-A non-B hepatitis and development of tests for these agents, idenfification and avoidance of blood from donors implicated in PTH cases, development of methods for immunizing transfused patients against the various agents responsible for PTH, and use of frozen-washed red blood cells for transfusion. Efforts to develop and/or evaluate these various approaches are currently being actively pursued in many laboratories.
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PMID:The clinical problem of hepatitis transmission;. 79 7

Screening for hepatitis B antigen (HB-sAg) in the serum of blood donors and exclusion of antigen-positive blood units have reduced the frequency of post-transfusion hepatitis but several cases of hepatitis B still occur in association with transfusions. One explanation for this is probably that HB-sAg is not an indicator of infectivity. Thus healthy carriers of the antigen seem to have low infectivity while carriers with chronic liver disease as well as donors incubating hepatitis B probably present a great risk.
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PMID:Hepatitis B antigen and prevention of post-transfusion hepatitis B. 80 65


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