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)

Immune electron microscopy was used to examine the morphological composition of HBsAg-containing structures in 20 patients with acute serum hepatitis (ASH) and severe accompanying disease in whom HBsAg had been detected by the gel precipitation test for a long time, and in 7 patients with HBsAg-positive chronic active hepatitis (CAH) developing after ASH. Small spherical particles were the predominant form of HBsAg-containing structures in all the sera. Among ASH patients, a significant number of tubular forms and Dane particles were detected mainly in patients with severe accompanying diseases. No correlation between the appearance of a large number of Dane particles and tubural forms and the severity of the disease in ASH was established. In CAH, tubular forms and Dane particles in large numbers were found only in patients with long periods after ASH. Large numbers of Dane particles in all the examined patients were combined with a large number of tubular forms.
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PMID:[Morphological makeup of the structures containing HBsAg in the blood of acute and chronic serum hepatitis patients]. 43 42

Serum levels of hepatitis B virus specific DNA polymerase and hepatitis B e antigen were studied serially in 34 patients with hepatitis B virus infection--20 who had the acute illness and recovered, seven who died with fulminant disease, three who died as a result of subacute hepatic necrosis, and four who went on to develop chronic active hepatitis. DNA polymerase activity was present in 16 (80%) and HBeAg in 13 (65%) of the uncomplicated cases at presentation and in all of those patients from whom the initial sample was obtained before the peak in aminotransferase. Both markers disappeared after 30 days from the onset but DNAP remained persistently positive during a follow-up period of four to 10 months in the four patients who progressed to chronic hepatitis. These results indicate that DNAP and HBeAg are transiently present in all cases of acute hepatitis B. Only their persistence after the acute episode could represent a useful prognostic marker of chronically. In this respect, DNAP was more reliable in our patients than HBeAg. In uncomplicated acute hepatitis, the peak in DNAP levels, which defines the time of maximum virus replication in the liver, preceded the peak in aminotransferase levels. Among the 10 patients who developed massive liver damage after hepatitis B infection, DNAP was detected in five of the seven with fluminant hepatitis, with enzyme levels that were comparable with those observed in uncomplicated acute hepatitis and presentation, but not in the cases of subacute hepatic necrosis. These findings are consistent with the hypothesis that in hepatitis B infection, liver damage, whatever the severity, is not directly related to the degree of virus replication.
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PMID:Changes in hepatitis B virus DNA polymerase in relation to the outcome of acute hepatitis type B. 43 51

Lymphocytes from patients with HBs-Ag-positive and -negative acute, chronic-persistent, and chronic-active hepatitis, from healthy controls and from patients with alcoholic liver cirrhosis were tested under standardized conditions. These included use of a single charge of Phytohemagglutinin (PHA-P) dissolved and diluted in one operation, of a single pool of homologous serum of the major blood group AB found free of HBs-Ag and cytotixic factor, and elaboration of PHA dose response curves in the presence of autologous and homologous serum in each case examined. During the early phase of acute virus hepatitis B and non-B, and in HBs-Ag-positive chronic persistent and active hepatitis, hyperresponsiveness of lymphocytes to PHA was observed independently of the source of the serum present in the culture. Lymphocyte responsiveness returned to normal in the later phase of acute hepatitis and depressed in alcoholic liver cirrhosis and in cases of HBs-Ag-positive chronic active hepatitis in which cirrhosis had developed. Although the cause of these alterations in lymphocyte responsiveness is not completely understood, the central role of a primary change of the lymphocytes themselves affecting their ability to react to PHA seems probable.
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PMID:Lymphocyte proliferation to phytohemagglutinin (PHA) in hepatitis B antigen-positive and -negative hepatitis. 44 26

Fibrosing alveolitis is described in a 22 year old woman with immunoglobulin A (IgA) deficiency and hepatitis B surface antigen (HBsAg)-associated chronic active hepatitis. At lung biopsy HBsAg was detected by indirect immunofluorescence in the alveolar space but not in the septal fibrosis. We discuss the possible relationships between IgA deficiency on the one hand, and HBsAg-associated lung and liver diseases on the other hand.
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PMID:Fibrosing alveolitis and hepatitis B surface antigen-associated chronic active hepatitis in a patient with immunoglobulin A deficiency. 44 62

Two patients with histologically verified acute hepatitis but without any serological evidence of hepatitis A or hepatitis B infection are described. In both cases the acute attack of hepatitis type 'non-A, non-B' progressed histologically and clinically to chronic active hepatitis within a two-year period. One of the patients died from liver insufficiency a year later, while the other is still alive after eight years of follow-up. The two cases illustrate that a progression of acute hepatitis 'non-A, non-B' to chronic liver disease may occur just as has been reported for hepatitis B infection.
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PMID:Progression of hepatitis non-A, non-B to chronic active hepatitis: a histological follow-up of two cases. 44 68

Twenty-six untreated patients with chronic persistent hepatitis were followed prospectively for one to 17 years (mean 5.6 years). The patients developed no clinical features of chronic liver disease. Raised serum transaminase levels were usually, but not consistently, the only biochemical abnormality; gamma globulin values were normal. Serum markers of past or present hepatitis B infection were found initially in 14 patients: another two developed markers during their follow-up. Nine patients progressed to a mild or moderate chronic active hepatitis as shown by serial needle liver biopsies but there was no evidence of cirrhosis. This progression was not associated with any clinical or biochemical deterioration. Seven of these patients had presented with insidious symptoms, seven had serum markers of hepatitis B infection, and the four who were HBsAg positive had relatively lower serum HBsAg concentrations than did those patients who continued with chronic persistent hepatitis.
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PMID:Chronic persistent hepatitis: hepatitis B virus markers and histological follow-up. 46 67

Immune complexes (IC) were investigated in sera from 208 individuals with various clinical types of viral hepatitis diagnosed by clinical and laboratory criteria, including liver biopsy. Immune complexes were assessed by platelet aggregation (PI A) and by radioimmunoassay (RIA). The data were related to autoimmune phenomena (especially rheumatoid factors) and to the role that the IgM class of hepatitis B (HB) antibody might have in IC formation. Although the highest frequency of P1 A was in the few sera from patients with cirrhosis or hepatoma, the next highest was in sera from acute hepatitis patients (71%), and the lowest in sera from chronic active (57%) and chronic persistent (46%) hepatitis patients. A proportional number of patients with IC's were positive for hepatitis B surface antigen (HBs). A parallel prevalence was noted between P1 A and autoantibodies, with anti-Ig's being found more frequently in sera from acute hepatitis and chronic active hepatitis patients. The relationship between RIA results for complexes and RIA results for anti-IgG was inverse, as though anti-IgG interfered with IC reactivity by RIA. Anti-IgM pre-incubated with sera increased the amount of P1 A in sera from patients with acute hepatitis as well as in those from patients with chronic persistent hepatitis, suggesting a more frequent IgM involvement in IC's in these diseases than in chronic active hepatitis. Whereas liver cell damage in acute and active hepatitis may reflect elevated autoantibodies, the IgM class of HBs antibody may be involved in acute as well as chronic persistent hepatitis.
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PMID:Autoimmune implications of immune complexes in clinical variants of hepatitis B. 49 83

Eight patients with chronic hepatitis B infection (seven with chronic active hepatitis and one with chronic persistent hepatitis) were treated with daily intramuscular injections of human leucocyte interferon for periods of 5 to 8 weeks and in one case for 5 months. In one patient there was a marked fall in virus-associated DNA polymerase activity and in the number of DNA containing viral particles during each of two courses of interferon. Hepatitis Be antigen (HBeAg) also disappeared, the aspartate transaminase levels fell and liver histology improved. In the four other patients with detectable DNA polymerase activity there was an early fall but this was transient and in one of these patients there was a continuing rise in activity despite treatment. One other patient became HBeAg negative but hepatitis B surface antigen (HBsAg) titres were mostly unaffected by treatment. A marked decrease in T-lymphocyte mediated cytotoxicity towards HBsAg coated target cells was demonstrated and raises the possibility that an immunosuppressant action of interferon may offsets its direct anti-viral action but may also account for the improvement in liver function which occurred in some patients.
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PMID:Effects of human leucocyte interferon on hepatitis B virus replication and immune responses in patients with chronic hepatitis B infection. 50 26

372 children with suspected liver disease were examined for serum HBsAg. Six (three boys, three girls) were found to be positive (1.6%). Further studies of these patients for up to three and a half years revealed elimination of HBsAg in one case only. Biopsies were performed in five patients. Three showed mild chronic hepatitis (two chronic persistent hepatitis, one unspecific reactive hepatitis). Chronic aggressive hepatitis was diagnosed in one patient. One child seemed to be normal on light microscopy, but the findings on electron microscopy were abnormal, the liver cell nuclei being filled with core particles. Two thirds of the family contacts of these children showed hepatitis B marker. Two pregnancies were observed in HBsAg-positive mothers. An infection of the babies was not demonstrable.
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PMID:[Hepatitis B markers in paediatric patients (author's transl)]. 51 42

Thirty-five male patients with decompensated hepatosplenic schistosomiasis were longitudinally studied and divided into 3 Groups; with hepatitis B surface antigen (HBsAg) or antibody (anti-HBs) and a control group negative to both. Patients with HBsAg were persistently carrying the antigen as estimated by radioimmunoassay (RIA) for up to 3 years and when compared with the other 2 groups, they had significantly higher serum glutamic transaminases, their liver biopsy showed more destructive liver cell lesions in the form of chronic active hepatitis or liver cirrhosis, they were refractory to diuretic treatment and had higher mortality rate (64% in 3 years compared to 22% and 33% in the other 2 groups). The majority of patients with dual infection are at greater risk in spreading hepatitis B as they proved to carry the 'e' antigen.
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PMID:Chronic hepatitis B antigenaemia in patients with hepatosplenic schistosomiasis. 52 49


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