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Hepatitis B Core Antibody (hepatitis + b_core_antibody)
Selected AbstractsFulminant hepatitis after allogenic bone marrow transplantation caused by reactivation of hepatitis B virus with gene mutations in the core promotor regionEUROPEAN JOURNAL OF HAEMATOLOGY, Issue 3 2006Kiyoshi Kitano Abstract:, Under immunosuppressive conditions after hematopoietic stem cell transplantation (HSCT), even if hepatitis B virus (HBV) antigen is negative but hepatitis B surface antibody (HBsAb) or hepatitis B core antibody (HBcAb) is presented, HBV reactivates and sometimes causes fulminant hepatitis. However, it remains unclear which patients will develop fulminant hepatitis, or whether fulminant hepatitis is caused by host-related factors or by virus-related factors. A 30-yr-old man with a history of aplastic anemia since 3 yr of age underwent allogenic BMT, when HBsAb and HBcAb were positive but HBs antigen (HBsAg) was negative. The donor was negative for HBsAg, HBsAb and HBcAb. After transplantation, the patient was complicated by acute graft-vs.-host disease (GVHD), cytomegalovirus infection, intestinal thrombotic microangiopathy and aspergillus colitis. Chronic GVHD was well controlled by FK506 and prednisolone. Twenty months after transplantation, the patient was admitted with general fatigue and liver dysfunction and was found to be positive for HBsAg and HBeAg. His serum HBV-DNA level was >8.8 log of the genome equivalent (LGE)/mL. Therefore, he was diagnosed as having hepatitis B caused by HBV reactivation and 100 mg/d lamivudine treatment was started. However, jaundice and hepatic failure deteriorated and became fatal. On analysis of the HBV-DNA, two adjacent gene mutations in the core promoter region (T1762/A1764) were detected. Increased replication of the mutated HBV might have caused HBV reactivation which progressed to fulminant hepatitis. [source] Double-dose double-phase use of second generation hepatitis B virus vaccine in patients after living donor liver transplantation: Not an effective measure in transplant recipientsHEPATOLOGY RESEARCH, Issue 1 2009Noriyo Yamashiki Aims:, Post-transplant active immunization for chronic hepatitis B patients has been attempted in several studies with controversial results. We assessed the effect of a double-dose double-phase vaccination regimen among partial living donor liver recipients. Methods:, Eighteen patients who underwent liver transplantation (LT) for chronic hepatitis B and two non-hepatitis B virus (HBV)-infected patients who received hepatitis B core antibody (HBcAb)-positive donor organs were recruited 18,78 months after LT. All were on hepatitis B immunoglobulin (HBIG) mono-prophylaxis before and throughout vaccination, to maintain hepatitis B surface antibody (HBsAb) titers of more than 100 IU/mL. Recombinant hepatitis B surface antigen vaccine (40 µg) was administered intramuscularly during weeks 0, 4, 8, 24, 28 and 32. Results:, The patients consisted of 15 males and five females with a median age of 52 (39,59) years. None developed a sufficient HBsAb titer above 500 IU/mL by week 48. In two patients whose maximum HBsAb titer increased to above 300 IU/mL, we attempted to skip HBIG, but shortly thereafter the titer dropped below 100 IU/mL and HBIG administration was resumed. Although the HBIG dose was reduced during and after vaccination, cessation of administration was not achieved. Conclusion:, Double-dose double-phase use of second generation recombinant vaccine was not effective in this study population. The selected population should be targeted for a conventional vaccine regimen, and different approaches, such as strong adjuvant or pre-S containing protein, should be further tested in a larger number of patients after LT for chronic hepatitis B. [source] Efficacy and long-term immunogenicity of hepatitis B vaccine in haemodialysis patientsINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 3 2009A. Ramezani Summary Background:, Hepatitis B vaccine is effective in protection against hepatitis B virus (HBV) infection in haemodialysis (HD) patients, but the antibody response is variable in this population and the persistence of immunity in them remains largely unknown. In this study we aimed to evaluate the efficacy and long-term immunogenicity of hepatitis B vaccine in HD patients. Methods:, In this study, we initially offered HBV vaccination as double dose, four vaccine series schedule (40 ,g injections intramuscularly in the deltoid muscle at 0, 1, 2 and 6 months) to 54 HD patients who were negative for hepatitis B core antibody and did not receive any dose of HBV vaccine previously. Serum levels of hepatitis B surface antibody (anti-HBs) tested 1,2 months after completion of vaccination. Then we follow the patients up to 1 year after primary vaccination to evaluate the persistence of immunity (as indicated by serum levels of anti-HBs higher than or equal to 10 IU/l). Results:, After primary vaccination, 87% of patients developed anti-HBs levels above 10 IU/l. 27.8% and 59.2% of them were weak responders and high responders respectively. 13% of patients were non-responders. After 1-year follow-up, 18.18% of responders had lost their anti-HBs (transient responders). All of them were initially in weak responders group and had lower anti-HBs levels. Conclusion:, We found an average percentage of seroconversion after primary HBV vaccination in HD patients. Our study also supported this fact that an antibody titre above 100 IU/l following primary vaccination is necessary to maintain that level of antibody 1 year later. [source] Occult hepatitis B virus infection: a covert operationJOURNAL OF VIRAL HEPATITIS, Issue 1 2010F. B. Hollinger Summary., Detection of occult hepatitis B requires assays of the highest sensitivity and specificity with a lower limit of detection of less than 10 IU/mL for hepatitis B virus (HBV) DNA and <0.1 ng/mL for hepatitis B surface antigen (HBsAg). This covert condition is relatively common in patients with chronic hepatitis C virus (HCV) that seems to exert some influence on the replicative capacity and latency of HBV. Detection of virus-specific nucleic acid does not always translate into infectivity, and the occurrence of primer-generated HBV DNA that is of partial genomic length in immunocompetent individuals who have significant levels of hepatitis B surface antibody (anti-HBs) may not be biologically relevant. Acute flares of alanine aminotransferase (ALT) that occur during the early phase of therapy for HCV or ALT levels that remain elevated at the end of therapy in biochemical nonresponders should prompt an assessment for occult hepatitis B. Similarly, the plasma from patients with chronic hepatitis C that is hepatitis B core antibody (anti-HBc) positive (ħanti-HBs at levels of <100 mIU/mL) should be examined for HBV DNA with the most sensitive assay available. If a liver biopsy is available, immunostaining for hepatitis B surface antigen (HBsAg) and hepatitis B core antigen (HBcAg) should be contemplated and a portion of the sample tested for HBV DNA. This is another reason for optimal collection of a specimen (e.g. two passes with a 16-guage needle under ultrasound guidance). Transmission of HBV to immunosuppressed orthotopic liver transplant recipients by donors with occult hepatitis B (OHB) will continue to occupy the interests of the transplant hepatologist. As patients with OHB may have detectable HBV DNA in serum, peripheral blood mononuclear cells (PBMC) and/or liver that can be reactivated following immunosuppression or intensive cytotoxic chemotherapy, the patient needs to be either monitored or treated depending on the pretreatment serological results such as an isolated anti-HBc reaction or a detectable HBV DNA. [source] Transmission of hepatitis B infection from hepatitis B core antibody,positive liver allografts is prevented by lamivudine therapyLIVER TRANSPLANTATION, Issue 6 2001Andy S. Yu Donor shortage has led to the use of hepatitis B core antibody (anti-HBc)-positive (anti-HBc+) liver allografts for patients in need of relatively urgent orthotopic liver transplantation (OLT). Because anti-HBc+ allografts transmit hepatitis B virus (HBV) infection at a high rate, effective prophylaxis is required. We assessed the effectiveness of lamivudine in preventing HBV transmission by anti-HBc+ allografts. Between March 1996 and March 2000 at Cedars-Sinai Medical Center (Los Angeles, CA), 15 of 169 patients (8.9%) received liver allografts from anti-HBc+ donors. Six patients were hepatitis B surface antigen (HBsAg)+ (group 1), and 9 patients were HBsAg negative (HBsAg,; group 2) before OLT. All patients were administered lamivudine, 100 or 150 mg/d, orally after OLT. Patients who were HBsAg+ before OLT also were administered hepatitis B immunoglobulin (HBIG) prophylaxis. Hepatitis B serological tests were performed on all patients, and HBV DNA was determined in liver tissues in 10 patients. All 15 patients remained HBsAg, at their last follow-up 2 to 40 months (mean, 17 months) post-OLT. All patients in group 1 had antibody to HBsAg (anti-HBs) titers greater than 250 mIU/mL post-OLT (mean follow-up, 20 months; range, 7 to 40 months). Of the 2 patients in group 1 who underwent liver biopsy after OLT, 1 patient had detectable hepatic HBV DNA despite being anti-HBs+ and HBsAg,. Among the patients in group 2, none acquired anti-HBc or HBsAg. Hepatic HBV DNA was undetectable in the 7 patients in group 2 who underwent liver biopsy after OLT. Anti-HBc+ allografts can be safely used in patients who undergo OLT for chronic hepatitis B and susceptible transplant recipients if prophylaxis with combination HBIG and lamivudine or lamividine alone is administered after OLT, respectively. However, more data are needed to determine the efficacy of lamivudine monotherapy in preventing transmission of HBV infection from anti-HBc+ liver allografts to susceptible recipients. [source] Combined hepatocellular carcinoma and cholangiocarcinoma with components of mucinous carcinoma arising in a cirrhotic liverPATHOLOGY INTERNATIONAL, Issue 4 2006Daisaku Morita A rare autopsy case of combined hepatocellular and cholangiocarcinoma, occurring in a 54-year-old man with liver cirrhosis, is presented. Initial laboratory data included CEA 52.1 ng/mL, DUPAN-2 1600 U/mL, AFP 2 ng/mL, and negativity for hepatitis B surface antigen, hepatitis B early antigen and hepatitis B core antibody. Ultrasonography and CT scan showed a large tumor node in the liver with ringed enhancement, swelling of several para-aortic lymph nodes, and ascites. Clinically, it was not possible to determine whether the hepatic tumor was an intrahepatic cholangiocarcinoma or a metastatic carcinoma. Histologically, the primary lesion was composed solely of hepatocellular carcinoma (HCC) with a trabecular pattern, and the intrahepatic metastases consisted of a variable admixture of HCC and cholangiocarcinoma (CC) with excessive mucin production. Interestingly, the tumor cell cluster showing a trabecular growth pattern produced mucin and had immunohistochemical expression of hepatocyte, cytokeratins 7 and 8. It is concluded that these hepatic tumor cells had both HCC and CC characters. [source] | ||||||||||