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Review DNA-guided hepatitis B treatment, viral load is essential, but not sufficient. free! 2009
Bárcena Marugán R, García Garzón S. · Services of Liver-Gastroenterology, Ramón y Cajal Hospital, University of Alcalá, Ctra de Colmenar Km 9100, Madrid 28034, Spain. · World J Gastroenterol. · Pubmed #19152446 links to free full text
Abstract: Hepatitis B virus (HBV) infection is a global public health problem that concerns 350 million people worldwide. Individuals with chronic hepatitis B (CHB) are at increased risk of developing liver cirrhosis, hepatic de-compensation and hepatocellular carcinoma. To maintain undetectable viral load reduces chronic infection complications. There is no treatment that eradicates HBV infection. Current drugs are expensive, are associated with adverse events, and are of limited efficacy. Current guidelines try to standardize the clinical practice. Nevertheless, controversy remains about management of asymptomatic patients with CHB who are hepatitis B e antigen (HBeAg)-positive with normal alanine aminotransferase, and what is the cut-off value of viral load to distinguish HBeAg-negative CHB patients and inactive carriers. We discuss in detail why DNA level alone is not sufficient to begin treatment of CHB.
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Article [Adefovir therapy in hepatitis B virus infection.] 2006
Bárcena Marugán R. · Servicio de Gastroenterología. Hospital Ramón y Cajal. Madrid. España. · Gastroenterol Hepatol. · Pubmed #17298796 No free full text.
This publication has no abstract.
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Article Prevention of de novo hepatitis B infection in liver allograft recipients with previous hepatitis B infection or hepatitis B vaccination. 2002
Bárcena Marugán R, García-Hoz F, Vázquez Romero M, Nash R, Mateos M, González Alonso R, García González M, García Plaza A. · Gastroenterology Service, Hospital Ramón y Cajal, Madrid, Spain. · Am J Gastroenterol. · Pubmed #12358263 No free full text.
Abstract: OBJECTIVES: To assess de novo hepatitis B virus (HBV) transmission from liver donors with HBV serum markers (HBM) to their recipients and the need for HBV vaccination before liver transplantation. METHODS: A total of 108 orthotopic liver transplantations for nonviral disease and the risk of developing de novo hepatitis B based on HBMs before transplantation have been studied. Of the 108 patients, 94 met the study criteria and were divided into two groups: 27 who had HBMs before transplantation (from past infection or by previous vaccination) and 67 who had no HBM. Development of de novo hepatitis B was determined by analytical, serological, and histological parameters. RESULTS: No case (0%) of de novo hepatitis B was detected in the pretransplantation HBM group, whereas there were 10 cases (14.5%) in the other group (p < 0.005). CONCLUSIONS: The presence of pretransplantation HBM in liver transplant recipients protects these patients against the development of de novo hepatitis B. This is especially important considering that there is a high prevalence of donors with positive hepatitis B core antibody (especially in some countries), and that these donors transmit HBV infection to recipients without HBM in a significant number of cases. Thus, vaccination against HBV in patients who are candidates for liver transplantation is fundamental to avoid cases of de novo hepatitis B.
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Article [Risk of hepatitis B virus transmission from hepatitis B core antibody-positive liver donors] 2001
Bárcena Marugán R, García Garzón S, López San Román A, Peña González E, Nasha R, Férnandez Muñoz R, Mateos M, García Plaza A. · Gastroenterología, Hospital Ramón y Cajal, Madrid. · Med Clin (Barc). · Pubmed #11222157 No free full text.
Abstract: BACKGROUND: To study the hepatitis B virus (HBV) transmission from donors HBsAg-/AntiHBc+ to liver transplant recipients. PATIENTS AND METHOD: We studied retrospectively the HBV serological markers in 43 donors from our center and also the serological condition of the 41 recipients. The HBV serological markers were analyzed by ELISA and HBV DNA was detected by hybridation assays. RESULTS: 13 donors samples showed some HBV serological markers: 6 anti-HBc and anti- HBs (13.9%), 4 anti-HBc (9%) and 3 anti- HBs (6.9%). There were no cases of hepatitis B among liver recipients from donors with negative serological markers. Among the 13 recipients with HBV serological markers, 9 were followed during 39 (SD 17) months. The 5 recipients with no HBV markers, who received an anti- HBc+ with or without anti- HBs (100%) developed hepatitis B. The two liver recipients with anti-HBs solely, did not developed infection (0%). Of the 41 recipients, 15 had some HBV markers before transplant and two of them received an anti-HBc+ and did not develop the infection (0%). CONCLUSIONS: In our study, the prevalence of serological HBV infection in donors and recipients was of 30.2 and 31.7%, respectively. Anti-HBc with or without anti-HBs donors transmitted the HBV infection in all the cases (100%) to the susceptible recipients. The presence of anti-HBs in recipients protected these against the infection. Only the anti-HBs positive donors did not trasmit the HBV infection.
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