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B Virus Surface Antigen (b + virus_surface_antigen)

Distribution by Scientific Domains
Medical Sciences100%

Kinds of B Virus Surface Antigen

  • hepatitis b virus surface antigen
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    Selected Abstracts

    Characterization of Hepatitis B Virus Surface Antigen and Polymerase Mutations in Liver Transplant Recipients Pre- and Post-Transplant

    AMERICAN JOURNAL OF TRANSPLANTATION, Issue 6 2003
    Jeffrey J. Germer
    We evaluated serum samples from 18 chronic hepatitis B virus (HBV) patients who underwent liver transplantation for the presence of HBV polymerase and S gene mutations and HBV genotype using a new commercially available sequencing assay. All three patients with hepatitis B immune globulin (HBIG) treatment failure followed by nucleoside analogue treatment failure were infected with HBV genotype C; a pre-existing HBV S antigen (HBsAg) mutation (sD144A) was identified in one patient pretransplant, while sG145R mutations emerged in the other two patients post-transplant. These HBsAg mutations persisted for the duration of the study (5,6 years), despite the absence of HBIG administration for a 4,5-year period. Significant viral polymerase mutations (rtL180M and rtM204I/V) also emerged in all of these patients following treatment with lamivudine and/or famciclovir. Four of six patients with HBIG breakthrough without nucleoside analogue treatment failure yielded potentially significant HBsAg mutations post transplant. These data do not support previous reports highlighting the disappearance of HBsAg mutants in liver transplant recipients after discontinuation of HBIG. Determination of HBV genotype, as well as identification of HBV polymerase and S gene mutations in liver transplant candidates may be warranted to optimize HBV management strategies post transplant. [source]

    Serum ,-glutamyltransferase within its normal concentration range is related to the presence of diabetes and cardiovascular risk factors

    DIABETIC MEDICINE, Issue 9 2005
    D.-J. Kim
    Abstract Aims Although many studies have reported an association between serum ,-glutamyltransferase (GGT) and cardiovascular risk factors, the mechanism of this relationship has not been clarified. Methods The medical records of 29 959 subjects (age, median 48, range 14,90 years; 16 706 men, 13 253 women) who visited the Center for Health Promotion at Samsung Medical Center for a medical check-up between January 2001 and December 2003, were investigated. Subjects with hepatic enzyme/GGT concentrations higher than three times the upper limit of the reference range, a positive test for hepatitis C virus antibody, a positive test for hepatitis B virus surface antigen, currently taking anti-diabetic/anti-hypertensive/anti-lipid medication, or a white blood cell (WBC) count higher than 10 000 cells/ml, were excluded. The subjects of each gender were classified into five groups according to their serum GGT concentrations, into quartiles of the normal range of GGT (groups 1, 2, 3 and 4) and into a group with elevated GGT (group 5). Results As the group number increased (group 1 , 5), the frequencies of all of the following increased: (i) diabetes and impaired fasting glucose (IFG); (ii) hypertension, obesity (body mass index , 27 kg/m2), dyslipidaemia (LDL-cholesterol , 4.1 mmol/l and/or triglyceride , 2.46 mmol/l, or HDL-cholesterol < 1.16 mmol/l); (iii) metabolic syndrome. Moreover, these significant relationships between GGT concentrations within its normal range and the presence of diabetes/IFG, hypertension, obesity, dyslipidaemia, and metabolic syndrome persisted after adjusting for several clinical and biochemical variables and for the presence of fatty liver based on ultrasonographic findings. Odds ratios (95% CI) for group 4 (highest quartile of normal range of GGT) vs. group 1 (lowest quartile of normal range of GGT); the referent group, were 3.16 (2.15,4.65) for diabetes, 2.24 (1.73,2.90) for IFG, 1.93 (1.59,2.33) for obesity, 1.38 (1.23,1.55) for dyslipidaemia and 2.88 (2.28,3.65) for metabolic syndrome in men. In women, the odds ratios were 2.72 (1.34,5.52), 3.67 (2.26,5.97), 2.10 (1.61,2.74), 1.80 (1.58,2.04) and 3.57 (2.52,5.07), respectively. Conclusions Our data show that, even within its normal range, serum GGT concentrations are closely associated with the presence of diabetes and cardiovascular risk factors, and that these associations are independent of a fatty liver by ultrasonography. [source]

    Differential DNA methylation associated with hepatitis B virus infection in hepatocellular carcinoma

    INTERNATIONAL JOURNAL OF CANCER, Issue 6 2007
    Pei-Fen Su
    Abstract Gene inactivation through DNA hypermethylation plays a pivotal role in carcinogenesis. This study aimed to profile aberrant DNA methylation in different stages of liver disease, namely noncirrhosis, cirrhosis and hepatocellular carcinoma (HCC), and also to clarify the influence of hepatitis B virus (HBV) infection on the aberrant DNA methylation in HCCs. Promoter methylation in p14ARF, p16INK4a, O6 -methylguanine-DNA methyltransferase (MGMT), glutathione S -transferase pi (GSTP1) and E-cadherin (E-Cad) genes of 58 HCCs paired with adjacent nontumorous tissues was assayed by methylation-specific PCR. HBV infection was determined using a hepatitis B virus surface antigen (HBsAg) serological assay. The frequency of p16INK4a promoter methylation increased from noncirrhotic, cirrhotic, to HCC tissues (noncirrhotic vs. HCC, p < 0.001), while that of GSTP1 promoter methylation increased in cirrhotic tissues compared to noncirrhotic ones (p = 0.029). The frequency of GSTP1 promoter hypermethylation is significantly higher in HCC than in nontumorous tissues (p = 0.022) from HBsAg-positive patients, but not the HBsAg-negative controls (p = 0.289). While the frequency of E-Cad promoter hypermethylation remained high in both nontumorous tissues and HCCs from HBsAg-positive patients (p = 0.438), it was lower in HCCs than in nontumorous tissues from HBsAg-negative patients (p = 0.002). In contrast, the frequency of p16INK4a, MGMT and p14ARF promoter hypermethylation in HCCs was unrelated to HBsAg status. In conclusion, aberrant DNA methylation may begin at different stages of liver disease in a gene-dependent manner. Moreover, HBV infection may enhance or maintain GSTP1 and E-Cad promoter methylation and thereby affect hepatocarcinogenesis. © 2007 Wiley-Liss, Inc. [source]

    Prospective study on the risk of hepatocellular carcinoma among hepatitis C virus-positive blood donors focusing on demographic factors, alanine aminotransferase level at donation and interaction with hepatitis B virus

    INTERNATIONAL JOURNAL OF CANCER, Issue 6 2004
    Hideo Tanaka
    Abstract The risk for hepatocellular carcinoma (HCC) among asymptomatic hepatitis C virus (HCV) carriers is not well understood. A community-based prospective study was conducted for over 8 years by record linkage to the Osaka Cancer Registry. The subjects were 1,927 individuals who were positive for anti-HCV through screening for second-generation HCV antibody (passive hemagglutination assay: , 212) in voluntary blood donation. The risk factors for HCC and interaction between HCV and hepatitis B virus (HBV) infection were evaluated by including additional blood donors: 2,519 individuals positive for hepatitis B virus surface antigen (HBsAg) alone, 25 positive for both anti-HCV and HBsAg, 150,379 negative for both anti-HCV and HBsAg. The incidence of HCC (/105 person-years) among the HCV-positive individuals increased with age in both genders, ranging from 68 to 1,306 among those aged 45,74 years. In the HCV-positive individuals, the cumulative risk of developing HCC between the ages of 40 and 74 year was 21.6% among males and 8.7% among females. A stepwise increase in risk was noted as the serum alanine aminotransferase level increased or serum cholesterol level at baseline decreased in multivariate Cox proportional hazard analysis. The 9-year cumulative incidence of HCC among individuals positive for HCV alone, those positive for HBsAg alone and those positive for both was 3.0%, 2.0% and 12.0%, respectively. The age-and-sex-adjusted rate ratio was 126, 102 and 572, respectively, when those negative for both were used as a reference. The results demonstrate an increased risk for HCC among asymptomatic HCV-positive individuals in Japan. Coinfection with HBV and HCV carried a superadditive risk for HCC. © 2004 Wiley-Liss, Inc. [source]

    Treatment of hepatitis D

    JOURNAL OF VIRAL HEPATITIS, Issue 1 2005
    G. A. Niro
    Summary., Delta virus related chronic hepatitis is difficult to treat. The response to , -interferon (IFN), which still represents the only therapy for chronic hepatitis D, varies widely and occurs at different times from the beginning of treatment. The rate of response is proportional to the dose of IFN, with 9 million units (MU) three times a week being more effective than 3 MU thrice weekly. Sustained responses are unusual and are accompanied by the clearance of serum hepatitis B virus surface antigen (HBsAg), seroconversion to anti-HBs and improvement of liver histology. Although disease of a short-standing may respond better to therapy, clear predictors of response are still unidentified. Besides IFN, other therapeutic approaches such as immunosuppressive drugs, acyclovir, ribavirin and thymosin, have been unhelpful. Available evidence does not support the use of deoxynucleotide analogues. Famciclovir has no effect on disease activity and hepatitis D virus (HDV)-RNA levels. Twelve- or 24-month lamivudine treatment does not significantly affect biochemical, virological or histological parameters. Pegylated-IFN could represent a reasonable therapeutic option in the long-term treatment required for chronic hepatitis D. Antisense oligonucleotides and prenylation inhibitors hold promise as therapeutic agents of the future. Liver transplantation provides a valid option for end-stage HDV liver disease; the risk of re-infection is lower for HDV than for HBV under long-term administration of hyperimmune serum against HBsAg. Molecularly tailored drugs capable of interfering with crucial viral replicative processes of HDV appear to be the best prospect in the treatment of hepatitis D. [source]

    Correlation of clinical characteristics with detection of hepatitis B virus X gene in liver tissue in HBsAg-negative, and HCV-negative hepatocellular carcinoma patients

    LIVER INTERNATIONAL, Issue 5 2002
    Yoichiro Higashi
    Abstract: Purpose: We studied the clinical features and the etiology of hepatitis B virus surface antigen (HBsAg)-negative and antibody to hepatitis C virus (anti-HCV) negative patients with hepatocellular carcinoma. Methods: A total of 550 patients, hospitalized with an initial diagnosis of HCC were retrospectively studied. Eighty-one of these patients were HBsAg-positive (HB group), 404 patients were anti-HCV positive (HC group). The other 65 patients were negative for both HBsAg and for anti-HCV (NBNC group). We purified HBV-X gene from HCC or non-tumorous liver tissue of 23 NBNC patients using PCR. Results: Clinical features of NBNC as compared with HB and HC patients were as follows, respectively: non-cirrhosis rate (%): 57,37,15 (P = 0.02 for HB, P < 0.00001 for HC), the proportion of patients with normal ALT concentrations (%): 59,28,10 (P = 0.0002 for HB, P < 0.00001 for HC). Forty of 59 NBNC patients (68%) had anti-HBs and/or anti-HBc (healthy controls: 29%, P < 0.00001) and two of 56 had serum HBV DNA. Twelve of 23 NBNC patients had HBV-X gene in HCC and/or non-cancerous liver tissues (52%). None of 52 had serum HCV RNA. Conclusions: The NBNC patients with HCC had a higher frequency of non-cirrhotic liver without liver injury. The presence of the HBV-X gene in HCC suggests a possible role of past HBV infection in the development of HCC. About half of NBNC HCC is associated with seronegativity for HBsAg and positivity for the HBV-X gene in liver tissue. [source]