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Bethel, AK, United States

McMahon B.J.,Liver Disease and Hepatitis Program | McMahon B.J.,Centers for Disease Control and Prevention
Clinics in Liver Disease | Year: 2010

In this article, the 4 phases of chronic HBV infection are reviewed and the factors that are associated with disease progression and the development of hepatocellular carcinoma (HCC) and cirrhosis are discussed. Also discussed is what is known to date about how to identify persons at the highest risk of developing HCC and/or cirrhosis. Finally, ways in which the natural history can be altered by hepatitis B vaccination and identification, close monitoring, and appropriate treatment of chronically infected individuals are reviewed. © 2010 Elsevier Inc. Source


McMahon B.J.,Liver Disease and Hepatitis Program
F1000 Medicine Reports | Year: 2010

In the past two years, several national and international bodies have made recommendations and published updated practice guidelines for hepatitis B. In addition, new drugs have become available for treatment of hepatitis B. This article will review the new recommendations for screening for hepatitis B and for first-line antiviral medications to use for treatment. In addition, I will discuss the recent recommendations on treating hepatitis B and human immunodeficiency virus co-infection and the screening of people receiving immunosuppressive therapy. © 2010 Medicine Reports Ltd. Source


McMahon B.J.,Liver Disease and Hepatitis Program
Medical Clinics of North America | Year: 2014

Over 400,000 people worldwide are chronically infected with hepatitis B virus (HBV), are at increased risk of developing hepatocellular carcinoma (HCC) and cirrhosis. HBV infected persons need regular lifelong follow-up. Candidates for antiviral therapy include patients with moderate-to-severe liver disease as determined by elevated alanine aminotransferase and/or liver biopsy and elevated HBV DNA levels above 2000 IU/mL, per evidenced-based guidelines. Pegylated interferon, tenofovir and entecavir are the first line drugs of choice for those needing treatment. All patients undergoing cancer chemotherapy or immunosuppressive therapy should be screened for hepatitis B surface antigen (HBsAg) and given HBV antiviral prophylaxis if positive. © 2014 Elsevier Inc. Source


Kowalec K.,Public Health Agency of Canada | Kowalec K.,University of British Columbia | Minuk G.Y.,University of Manitoba | Borresen M.L.,Statens Serum Institute | And 5 more authors.
Journal of Viral Hepatitis | Year: 2013

Hepatitis B virus (HBV) infection is highly prevalent in circumpolar indigenous peoples. However, the clinical outcome is extremely variable, such that while hepatocellular carcinoma (HCC) is uncommon in Canadian Inuit, the incidence of HCC is slightly higher in Greenlanders than in Danes, and it is especially high in Alaskan Native people infected with HBV genotypes F (HBV/F) and C (HBV/C). These differences may be associated with the genomic variability of the predominant HBV genotype in each group. The purpose of this study was to determine the rate, nature and regional susceptibility of HBV genomic mutations among circumpolar indigenous individuals. Paired serum samples, separated by 5-6 years, were analysed from Canadian and Greenlandic Inuit infected with HBV genotype B6 (HBV/B6) and HBV/D, respectively, and from Alaskan Native people infected with HBV/F, each having subsequently developed HCC. Phylogenetic and mutational analyses were performed on full-genome sequences, and the dynamic evolution within the quasispecies population of each patient group was determined by clonal analysis of the non-overlapping core coding region. Mutations associated with severe outcomes predominated in HBV/F, mostly within the precore/core and PreS1 region. HBV/B6 genomes exhibited higher diversity compared to HBV/D and HBV/F, particularly within the core coding region. Thus, differing mutational profiles and genetic variability were observed among different HBV genotypes predominating in circumpolar indigenous patients. The unusual observation of persistently high genetic variability with HBV/B6 despite clinical inactivity could be due to the evolution of a host-pathogen balance, but other possible factors also need to be explored. © 2012 Blackwell Publishing Ltd. Source


Tohme R.A.,Centers for Disease Control and Prevention | Bulkow L.,Centers for Disease Control and Prevention | Homan C.E.,Liver Disease and Hepatitis Program | Negus S.,Liver Disease and Hepatitis Program | McMahon B.J.,Centers for Disease Control and Prevention
Journal of Clinical Virology | Year: 2013

Background: A high prevalence of reactivation of hepatitis B has been documented among immunosuppressed individuals in the inactive phase of chronic hepatitis B; However, the proportion of and the risk factors for reactivation are largely unknown among non-immunosuppressed persons. Objectives: Estimate the incidence rate of and risk factors for hepatitis B reactivation in a population-based cohort of persons in the inactive phase of chronic hepatitis B in Alaska. Study design: A cohort of 414 Alaska Native Persons in the inactive phase of hepatitis B (HBV DNA. <. 2000. IU/mL and normal alanine aminotransferase (ALT) for 12 months) was followed-up for 10 years. Reactivation of hepatitis B was defined as HBV DNA. ≥. 2000. IU/mL and ALT. ≥. 40. IU/L. Cox-proportional hazards regression models were used to identify factors associated with reactivation. Results: A total of 36 (9%) persons had reactivation during 2984 person-years of follow-up, with an annual incidence of 1.2%. Persons aged ≥50 years (1.8%) at study entry had the highest incidence rates of reactivation although incidence rates were not significantly different by age group. Risk factors for hepatitis B reactivation were male sex (Hazard Ratio (HR)=2.41; 95% Confidence Interval (CI): 1.17-4.96), HBV DNA. ≥. 1000. IU/mL at study entry (HR=7.61; 95% CI: 2.81-20.6), and HBV genotype B (HR=6.08; 95% CI: 1.32-28.0).Conclusions The incidence of hepatitis B reactivation was low during the 10 years of follow-up. However, given the higher risk of reactivation than their counterparts, males, and those with HBV DNA. ≥. 1000. IU/mL need to be followed-up more frequently. © 2013. Source

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