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At least 19 recordsLinked to original sources
PubMedDate not supplied

Current tests for antibody to hepatitis b core antigen used to screen donors for non-A, non-B hepatitis are comparable to the original radioimmunoassay for hepatitis B core antigen.

Prospective studies have shown a relationship between the transfusion of donor blood which is positive for antibodies to hepatitis B core antigen (anti-HBc) and an increased incidence of non-A, non-B hepatitis. The anti-HBc test was selected on the assumption that epidemiologic circumstances predisposing donors to hepatitis B infection also might favor exposure to non-A, non-B hepatitis. Current radioimmunoassays (RIA) and enzyme-linked immunoassays (EIA) for anti-HBc utilize hepatitis B core antigen (HBcAg) prepared by recombinant DNA technology, whereas the original RIA anti-HBc assay used HBcAg derived from hepatitis B virions. In the current study, 1329 sera were evaluated of which 23.3 percent were anti-HBc positive. The results indicate that sensitivity, specificity, and positive and negative predictive values of the current EIA and RIA tests for anti-HBc (Abbott Diagnostic Laboratories) are virtually identical to the original RIA test kit. In addition, all donor samples (128 specimens) administered to 57 cases of non-A, non-B hepatitis that were prospectively followed at Baylor College of Medicine for the Transfusion-Transmitted Viruses (TTV) Study group were retested with the EIA-recombinant anti-HBc assay. All 21 samples which were reactive in the original RIA anti-HBc test also were positive by the current EIA procedure. One sample was EIA positive/RIA negative, and 106 other samples were negative by both assays. Thus, commercial anti-HBc kits based on HBcAg derived by recombinant DNA technology, should retain their predictive value for reducing the incidence of non-A, non-B hepatitis as described in the prospective studies.

Antibodies, Viral↗
PubMed2000

Hepatectomy for hepatitis B-, hepatitis C-, and dual hepatitis B- and C-related hepatocellular carcinoma in Taiwan.

To evaluate the surgical results of patients with hepatitis B-, hepatitis C- and dual hepatitis B- and C-related hepatocellular carcinoma (HCC), we reviewed the clinical records 252 patients (196 men and 56 women) with complete profiles of hepatitis B and hepatitis C infection who had hepatectomies to treat HCC from March, 1992, to August, 1998. The patients were divided into four groups, 30 patients (11.9%) without either hepatitis B surface antigen or anti-hepatitis C antibody (N-HCC group), 133 patients (52.8%) with hepatitis B infection only (B-HCC group), 66 patients (26.2%) with hepatitis C infection only (C-HCC group), and 23 patients (9.1%) with dual hepatitis B and C infection (BC-HCC group). Compared with the patients in the other groups, the patients in the C-HCC group were older and had more severe cirrhotic change of the liver. The surgical complication rates and hospital mortalities in the C-HCC and BC-HCC groups were 30.3% and 12.1% and 30.4% and 17.4%, respectively, which were higher than those in the N-HCC (13.3%, 3.3%) and B-HCC (15.8%, 3.8%) groups. The mean disease-free survivals for the N-HCC, B-HCC, C-HCC, and BC-HCC groups were 31.4, 25.4, 38.9 and 13.8 months, respectively, with the difference between the four groups being significant (P < 0.05). However, the mean overall survival times, 38.3 months for the N-HCC group, 37.2 months for the B-HCC group, 52.1 months for the C-HCC group, and 32.7 months for the BC-HCC group, were not significantly different (P = 0.146). In conclusion, surgical treatments for HCC related to hepatitis C or dual hepatitis B and C infection were associated with a higher surgical complication rate and hospital mortality. Hepatocellular carcinoma related to dual hepatitis B and C infection recurred earlier after hepatectomy, but the overall survival of the four groups was not significantly different.

Adult↗
PubMed1992

Acute exacerbations of chronic type B hepatitis are accompanied by increased T cell responses to hepatitis B core and e antigens. Implications for hepatitis B e antigen seroconversion.

T cell proliferative responses to hepatitis B virus-encoded envelope antigen (S + preS2 + preS1), recombinant core antigen (HBcAg), and natural hepatitis B e antigen (HBeAg) were examined in 22 HBeAg-positive patients with chronic type B hepatitis and 17 healthy hepatitis B surface antigen (HBsAg) carriers. The results showed that HBeAg-positive patients had (a) higher levels of T cell responses to HBcAg/HBeAg than those of healthy HBsAg carriers (P less than 0.001 and P less than 0.01, respectively); (b) a further increase in these T cell responses during acute exacerbations (P less than 0.05 and P less than 0.05, respectively); (c) subsidence in the T cell responses to HBcAg/HBeAg after recovery from acute exacerbations and HBeAg seroconversion, whereas the responses would persist at high levels if the patients did not enter a clinical remission; and (d) low levels of T cell responses to S + preS2 + preS1 either before or after HBeAg seroconversion. The appearance of increasing T cell responses to HBcAg/HBeAg usually occurred in the early phase of acute exacerbations. These findings imply that HBcAg/HBeAg-specific T cells play an important role in the exacerbations of chronic hepatitis B and in HBeAg seroconversion. HBcAg/HBeAg-specific precursor T cell frequencies were serially studied in selected cases by limiting dilution assay. Elevation (two- to fourfold) of HBcAg/HBeAg-specific precursor T cell frequencies contributed to the increase of HBcAg/HBeAg-specific T cell proliferation during acute exacerbations.

Adult↗
PubMed1995

Failure to incriminate hepatitis B, hepatitis C, and hepatitis E viruses in the aetiology of fulminant non-A non-B hepatitis.

Sporadic non-A, non-B hepatitis is the most common indication for liver transplantation in patients presenting with fulminant and subacute liver failure. This study used serological, histological, and molecular biological techniques to examine specimens from 23 consecutive patients transplanted for sporadic non-A, non-B hepatitis. No evidence was found of hepatitis C virus, hepatitis E virus, or 'cryptic' hepatitis B virus infection.

Adolescent↗
PubMed2000

Recurrent hepatitis B, hepatitis C, and combined hepatitis B and C in liver allografts: a comparative pathological study.

Although recurrence of viral hepatitis in liver transplants is common, data comparing recurrent hepatitis B (HB), hepatitis C (HC), and co-existing dual hepatitis B and C (HB&C) are sparse. Posttransplantation liver biopsies, along with molecular, serological, immunohistochemical, and clinical data from 27 patients with pretransplantation diagnosis of chronic viral hepatitis, were reviewed. The patients were placed into 4 groups: Group I, with pretransplantation HB (n = 8); group II, with pretransplantation HC (n = 10); group III with pretransplantation HC and anti-HB surface or core antibody (n = 4); and group IV, with pretransplantation HB&C (n = 5). The histopathologic findings and patient outcome were compared in the 4 groups. A high rate of recurrence of viral hepatitis was seen for all 4 groups: Group I = 100%, group II = 90%, Group III = 100%, and group IV = 80%, with the mean (median) recurrence time of 308 (224), 82 (52), 61 (64), and 125 (70) days, respectively. The number of deaths (their median survival times) were: group I = 4 (374 days), group II = 4 (794 days), group III = 1 (1,143 days), and group IV = 5 (448 days). The earliest histological findings of lobular injury was the presence of acidophil bodies and Kupffer cell hyperplasia, the latter being more prominent in recurrent HC cases. Recurrent HB presented in 2 forms: early (before 150 days) with poor survival and with either severe necroinflammatory histology or with features of fibrosing cholestatic hepatitis, and delayed (after 150 days), with mild necro-inflammatory activity and prolonged survival. HC with or without anti-HB antibodies had early recurrence, but the course was slowly progressive. Patients with HB&C had recurrence of both viruses; however, the course was dictated by HB virus.

Hepatitis B, Chronic↗
PubMed1998

The sequential occurrence of viral mutations in a liver transplant recipient re-infected with hepatitis B: hepatitis B immune globulin escape, famciclovir non-response, followed by lamivudine resistance resulting in graft loss.

BACKGROUND/AIMS: The purpose of this study was to characterize the clinical, histological and virological events in an orthotopic liver transplant (OLT) recipient with recurrent hepatitis B infection who was initially managed with hepatitis B immune globulin (HBIg) and when viral recurrence occurred, with nucleoside analogue salvage therapy. The aims were to document the mutations occurring in the hepatitis B virus (HBV) polymerase gene as a consequence of HBIg escape, famciclovir non-response and subsequent lamivudine resistance. METHODS: Throughout the follow-up of 796 days, the patient was seen at least at 4-week intervals. Clinical, biochemical and virological data were registered according to protocol. HBV DNA was quantified throughout the treatment period. The viral polymerase gene was sequenced from serum samples collected at representative time intervals. Consecutive liver biopsies were scored according to the modified Knodell classification. RESULTS: Clinically, the patient was in excellent condition until the development of acute hepatitis during the lamivudine therapy period, 765 days post-OLT. Until this terminal event, serum transaminase activity was only 1-2 times the upper limit of normal with serum bilirubin and prothrombin time within the normal range. Subsequent liver biopsies showed chronic active hepatitis with no signs of fibrosis. The post-mortem biopsy showed severe acute hepatitis B with massive necrosis. The HBV polymerase gene was sequenced during HBIg, famciclovir and lamivudine treatment. One mutation I533L was detected during HBIg treatment. No amino acid changes were selected during famciclovir treatment. Three amino acid changes were selected while the patient was on lamivudine treatment, which include L533I, S559T and M550I. CONCLUSIONS: We have documented HBV recurrence in a liver transplant recipient with the emergence of a multidrug resistant HBV which caused graft loss. The primary resistance to famciclovir in spite of therapeutic penciclovir levels may be as a result of a combination of the mutations found in the polymerase region. After 300 days of lamivudine treatment, a drug-resistant population emerged which was associated with a greater than three log increase in HBV DNA and contributed to loss of graft function. This is the first report of such an adverse clinical outcome due to the emergence of a mutant virus as a consequence of immunoprophylactic and antiviral therapy in a liver transplant recipient.

2-Aminopurine↗
PubMed1989

[The relation of B- and non-A, non-B hepatitis virus--hepatitis B virus (HBV) DNA hybridization studies of the sera in non-A, non-B hepatitis].

Referring to informations of various international groups of investigators who regard the NANBH as HBV-variant the sera of 77 female patients with chronic NANBH and 28 acute phase sera of a NANBH serum bank were tested for HBV-DNA. The sera in question were such ones of a particularly well defined group of patients with unique parenteral source of infections. Though further ALAT attacks were observed, in none of the NANBH-sera HBV-DNA was proved as a sign of an active HBV-replication. This, like the absence of an immunity against the NANBH-virus after HBV-disease and the observed suppression of the HBV-DNA in NANBH-superinfection of HBV-carriers (virus interference), speaks against the hypothesis of a close genetic relationship between the two viruses.

Adult↗
PubMed2002

Genotype B hepatitis B virus is associated with severe icteric flare-up of chronic hepatitis B virus infection in Hong Kong.

OBJECTIVE: We aimed to investigate the association of viral genotype and the development of icteric flare-up (IF) in chronic hepatitis B virus (HBV) infection. METHODS: Twenty-one consecutive patients suffering from IF of chronic HBV infection, defined as elevation of ALT over five times the upper limit of normal, together with either bilirubin > 50 IU/L or elevated bilirubin plus PT > 3 s prolonged, were studied. Patients from three stages of HBV-related chronic liver disease were studied as controls: 1) asymptomatic carriers (31 patients), defined as persistent normal ALT for at least 2 yr; 2) active early cirrhosis (49 patients), defined as Child's A liver cirrhosis plus HBV DNA > 106 Eq/ml; and 3) decompensated cirrhosis (31 patients), defined as Child's B or C liver cirrhosis with complications. Restriction fragment length polymorphism was used for genotyping. RESULTS: Only genotype B and C HBV were identified in our studied cohort. Ninety-one percent of patients suffering from IF were infected by genotype B HBV (p < 0.001 vs asymptomatic carriers, early cirrhosis patients, and decompensated cirrhosis patients). On the contrary, genotype C HBV was the predominant strain at different stages of chronic liver disease; no statistical difference was found on the relative prevalence of genotype B/C HBV among asymptomatic carriers, early cirrhosis patients, and decompensated cirrhosis patients. CONCLUSIONS: Genotype B HBV is associated with IF among chronic HBV-infected patients in Hong Kong, whereas genotype C HBV is more prevalent at all stages of chronic liver disease. Our findings suggested that the two different HBV genotypes might have different pathogenic mechanisms of liver damage.

Adult↗
PubMed1994

Exclusion in liver by polymerase chain reaction of hepatitis B and C viruses in acute liver failure attributed to sporadic non-A, non-B hepatitis.

Hepatitis B and C viruses have been implicated in a few cases of acute liver failure attributed to sporadic (community acquired) non-A, non-B hepatitis, but reports are conflicting. We determined whether hepatitis B virus and hepatitis C virus were detectable in prospectively stored hepatectomies from seven British patients grafted for acute liver failure attributed to sporadic non-A, non-B hepatitis. For hepatitis B virus, we used nested polymerase chain reaction with primers to the core and surface regions. For hepatitis C virus, we used one round of reverse transcription polymerase chain reaction with primers to the 5' untranslated region and Southern hybridization using an internal oligonucleotide probe as well as nested PCR for the E1 region. Positive controls were native livers from two patients with unequivocal fulminant hepatitis B and from four patients with cirrhosis attributed to hepatitis C virus. Our negative findings suggest that, in the UK, acute liver failure attributed to sporadic non-A, non-B hepatitis most likely is caused by agent/s other than hepatitis B and C viruses.

Blotting, Southern↗
PubMed1983

Effect of short-term prednisone therapy on aminotransferase levels and hepatitis B virus markers in chronic type B hepatitis.

We have studied the effect of short-term high-dose prednisone therapy on aminotransferase levels and hepatitis B virus markers in 6 patients with chronic type B hepatitis. All showed a decrease in amino transferase levels during treatment. This was followed by a transient increase in aminotransferase levels after prednisone was discontinued. In 5 patients, there was a decrease in hepatitis B virus deoxyribonucleic acid polymerase activity at the time of postprednisone peak of aminotransferase levels. Three of them became transiently deoxyribonucleic acid polymerase negative. All the patients have remained hepatitis B e antigen-positive throughout the period of observation. We have also found transient deoxyribonucleic acid polymerase negativity unrelated to prednisone therapy in 2 patients with chronic type B hepatitis: in one during a superimposed episode of acute type A hepatitis, and in the other during a period of pronounced alanine aminotransferase elevation. We postulate that these periods of deoxyribonucleic acid polymerase negativity are due to a decreased number of hepatitis B virus-infected cells in the liver as a consequence of hepatic necrosis.

Adult↗
PubMed1985

Hepatic decompensation associated with hepatitis B e antigen clearance in chronic type B hepatitis.

To examine hepatic decompensation associated with acute exacerbation preceding hepatitis B e antigen clearance in chronic type B hepatitis, 376 patients with chronic hepatitis who were hepatitis B e antigen-positive were prospectively studied for up to 7 yr (mean 25 mo). Among the 165 patients who underwent hepatitis B e antigen clearance, 4 patients experienced hepatic decompensation and one of them eventually developed hepatic encephalopathy and died. The incidence of hepatic decompensation associated with hepatitis B e antigen clearance was 2.4%. We suggest that such an event in previously unrecognized chronic hepatitis B carriers could have been erroneously interpreted as acute or subacute hepatic failure, and that it might have been the result of a stronger enhancement of the host immune response.

Acute Disease↗
PubMed1996

The seroprevalence of hepatitis B, hepatitis C and human immunodeficiency virus infections in paediatric oncology patients in Turkey.

One hundred and two newly diagnosed children with malignancy followed up at the Pediatric Oncology Department of Ankara Oncology Hospital were investigated for hepatitis B, hepatitis C and human immunodeficiency virus markers. The ages ranged between seven months and 17 years with a median of 10 years; 62 were male. Twenty-four patients had Hodgkin's disease, 11 had non-Hodgkin's lymphoma and 67 patients had other solid tumours. Four patients had positive HBs-Ag, 15 developed immunity against hepatitis B and had anti-HBs antibodies. One patient had a previous infection with positive anti-HBc. Hepatitis C virus antibodies were positive in only one patient. HIV serology was negative in all patients. These results show the high prevalence of hepatitis B virus infection in paediatric oncology patients. In countries where hepatitis B is endemic, strict screening of blood donors, usage of disposable equipment and vaccination of patients is recommended. Although the incidence of hepatitis C and human immunodeficiency virus infections are rising, infection with hepatitis B is still by far the most common.

AIDS-Related Opportunistic Infections↗
PubMed1988

Reactivation of hepatitis B virus in anti-HBe-positive chronic active type B hepatitis: molecular and immunohistochemical studies.

The causes of acute clinical exacerbations, and the role of reactivation of hepatitis B virus (HBV) in 16 non-cirrhotic patients with chronic active type B hepatitis (CAH-B) negative for serum hepatitis B e antigen (HBeAg) but positive for anti-HBE, were studied by molecular hybridization and immunohistochemical methods. IgM antibody to hepatitis A virus (anti-HAV IgM) and antibody to delta agent (anti-delta) were negative in all. HBeAg reappeared transiently in only two patients. Serum hepatitis B virus (HBV) DNA levels increased during acute exacerbations in 14 patients (88%), and decreased after the episode. Cytoplasmic hepatitis B core antigen (HBcAg) expression was found in 9 out of 13 patients (69%) during acute exacerbation. By Southern blot hybridization, 5 of 6 (83%) liver tissues obtained during clinical exacerbations had free replicative forms of HBV DNA. In 20 control patients with no exacerbation, serum HBV DNA, HBcAg expression in hepatocytes and free replicative forms of HBV DNA were positive in 15% (3/20), 10% (2/20) and 25% (2/8), respectively--figures significantly lower than those of the group studied. We conclude that acute exacerbations sometimes seen in patients with anti-HBe-positive CAH-B in Taiwan are caused mainly by reactivation of HBV.

Adult↗
PubMed1991

Engerix-B hepatitis B vaccine (recombinant)/Smith, Kline & French.

Engerix-B [Hepatitis B Vaccine (Recombinant)], a product by SmithKline Biologicals, is a noninfectious recombinant DNA hepatitis B vaccine for immunization against infection caused by all known subtypes of hepatitis B virus. It provides a safe and well-tolerated vaccination regimen shown to confer immunity on the basis of anti-HBs antibody responses comparable with those of plasma-derived vaccines.

Clinical Trials as Topic↗
PubMed1997

Detection of hepatitis G virus RNA in patients with hepatitis B, hepatitis C, and non-A-E hepatitis by RT-PCR using multiple primer sets.

Hepatitis G virus(HGV)/GB virus C(GBV-C) is a newly identified virus associated with human hepatitis. The preliminary prevalence studies of HGV infection in Japan were entirely based on the detection of HGV RNA by RT-PCR. However, the selection of the different primer sets in such assay may influence sensitivity of the test because of the extensive genetic heterogeneity of HGV, and influence the estimation of the prevalence of HGV. To address this potential problem, we designed two primer sets from well conserved domains in the 5'NC and NS5 regions of HGV genome, and tested them together with the NS3-derived primer set in RT-PCR for their ability to detect HGV RNA in serial dilution of synthetic viral RNA templates. Subsequently, we used these three primer sets to detect HGV RNA in the sera of 371 Japanese patients with hepatitis B, hepatitis C, and non-A-E hepatitis. The results indicated that the primer set derived from the 5'NC region appeared to be most effective in detecting HGV RNA. The results also showed that only two out of the 126 patients (1.6%) with non-A-E hepatitis were positive for HGV RNA although the RNA were detected more frequently in patients with hepatitis B (2/38; 5.3%) and hepatitis C (17/207; 8.2%), suggesting that HGV is not a common causative agent for non-A-E hepatitis in Japan.

Base Sequence↗