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      Characteristics of Patients With Chronic Hepatitis B Virus Infection With Genotype E Predominance in Burkina Faso

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          Abstract

          Hepatitis B virus (HBV) genotype E (HBV‐E) accounts for the majority of chronic hepatitis B (CHB) infections in West Africa. We aimed to determine factors associated with HBV‐E‐induced hepatocellular carcinoma (HCC) in West Africa. Data on patients from Burkina Faso who were hepatitis B surface antigen positive (HBsAg+) and had CHB were analyzed. HBV viral load and hepatitis B e antigen (HBeAg) status were measured in 3,885 individuals with CHB without HCC (CHB HCC−) and 59 individuals with CHB with HCC (CHB HCC+). HBV genotyping was performed for 364 subjects with CHB HCC− and 41 subjects with CHB HCC+. Overall, 2.5% of the CHB HCC− group was HBeAg+ compared with 0% of the CHB HCC+ group. Of the 364 patients who were CHB HCC− with available genotyping, the frequencies of HBV genotypes E and C/E were 70.3% and 12.9%, respectively. Age (odds ratio [OR] for older age, 1.08; 95% confidence interval [CI], 1.06‐1.10 per 1‐year increase in age), male sex (OR, 2.03; 95% CI, 1.11‐3.69), and HBV viremia (OR, 1.48; 95% CI, 1.31‐1.67 per 1 log10 IU/mL) were each associated with HCC diagnosis. Patients with genotype E had a lower HBeAg prevalence (6.3% vs. 14.9%), lower HBV viral load, and higher prevalence of cirrhosis (14.5% vs. 4.8%) than patients with genotype C/E. Conclusion: HBV‐E is the most common circulating strain (70.3%) in West African patients. HCC was associated with older age, male sex, and high HBV viral load. It is expected that these results will further inform guidance on clinical management of HBV infection in West Africa.

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          EASL 2017 Clinical Practice Guidelines on the management of hepatitis B virus infection.

          Hepatitis B virus (HBV) infection remains a global public health problem with changing epidemiology due to several factors including vaccination policies and migration. This Clinical Practice Guideline presents updated recommendations for the optimal management of HBV infection. Chronic HBV infection can be classified into five phases: (I) HBeAg-positive chronic infection, (II) HBeAg-positive chronic hepatitis, (III) HBeAg-negative chronic infection, (IV) HBeAg-negative chronic hepatitis and (V) HBsAg-negative phase. All patients with chronic HBV infection are at increased risk of progression to cirrhosis and hepatocellular carcinoma (HCC), depending on host and viral factors. The main goal of therapy is to improve survival and quality of life by preventing disease progression, and consequently HCC development. The induction of long-term suppression of HBV replication represents the main endpoint of current treatment strategies, while HBsAg loss is an optimal endpoint. The typical indication for treatment requires HBV DNA >2,000IU/ml, elevated ALT and/or at least moderate histological lesions, while all cirrhotic patients with detectable HBV DNA should be treated. Additional indications include the prevention of mother to child transmission in pregnant women with high viremia and prevention of HBV reactivation in patients requiring immunosuppression or chemotherapy. The long-term administration of a potent nucleos(t)ide analogue with high barrier to resistance, i.e., entecavir, tenofovir disoproxil or tenofovir alafenamide, represents the treatment of choice. Pegylated interferon-alfa treatment can also be considered in mild to moderate chronic hepatitis B patients. Combination therapies are not generally recommended. All treated and untreated patients should be monitored for treatment response and adherence, and the risk of progression and development of complications. HCC remains the major concern for treated chronic hepatitis B patients. Several subgroups of patients with HBV infection require specific focus. Future treatment strategies to achieve 'cure' of disease and new biomarkers are discussed.
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            AASLD guidelines for treatment of chronic hepatitis B.

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              Risk of hepatocellular carcinoma across a biological gradient of serum hepatitis B virus DNA level.

              Serum hepatitis B virus (HBV) DNA level is a marker of viral replication and efficacy of antiviral treatment in individuals with chronic hepatitis B. To evaluate the relationship between serum HBV DNA level and risk of hepatocellular carcinoma. Prospective cohort study of 3653 participants (aged 30-65 years), who were seropositive for the hepatitis B surface antigen and seronegative for antibodies against the hepatitis C virus, recruited to a community-based cancer screening program in Taiwan between 1991 and 1992. Incidence of hepatocellular carcinoma during follow-up examination and by data linkage with the national cancer registry and the death certification systems. There were 164 incident cases of hepatocellular carcinoma and 346 deaths during a mean follow-up of 11.4 years and 41,779 person-years of follow-up. The incidence of hepatocellular carcinoma increased with serum HBV DNA level at study entry in a dose-response relationship ranging from 108 per 100,000 person-years for an HBV DNA level of less than 300 copies/mL to 1152 per 100,000 person-years for an HBV DNA level of 1 million copies/mL or greater. The corresponding cumulative incidence rates of hepatocellular carcinoma were 1.3% and 14.9%, respectively. The biological gradient of hepatocellular carcinoma by serum HBV DNA levels remained significant (P or =10,000 copies/mL) is a strong risk predictor of hepatocellular carcinoma independent of HBeAg, serum alanine aminotransferase level, and liver cirrhosis.
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                Author and article information

                Contributors
                nagalo.bolni@mayo.edu
                roberts.lewis@mayo.edu
                Journal
                Hepatol Commun
                Hepatol Commun
                10.1002/(ISSN)2471-254X
                HEP4
                Hepatology Communications
                John Wiley and Sons Inc. (Hoboken )
                2471-254X
                15 September 2020
                December 2020
                : 4
                : 12 ( doiID: 10.1002/hep4.v4.12 )
                : 1781-1792
                Affiliations
                [ 1 ] Division of Gastroenterology and Hepatology Mayo Clinic Rochester MN
                [ 2 ] Department of Biochemistry and Microbiology Pietro Annigonni Biomolecular Research Center Ouagadougou Burkina Faso West Africa
                [ 3 ] Division of Hematology and Medical Oncology Mayo Clinic Hospital Phoenix AZ
                [ 4 ] Genomics Research Center Academia Sinica Taipei Taiwan
                [ 5 ] Division of Infectious Diseases and Microbiology University of Pittsburgh Pittsburgh PA
                [ 6 ] Computational Sciences and Informatics Program for Complex Adaptive System Arizona State University Tempe AZ
                [ 7 ] College of Pharmacy University of Louisiana Monroe Monroe LA
                [ 8 ] Department of Health Sciences Research Mayo Clinic Jacksonville FL
                Author notes
                [*] [* ] Address Correspondence and Reprint Requests to:

                Lewis R. Roberts, M.B., Ch.B., Ph.D.

                Division of Gastroenterology and Hepatology

                Mayo Clinic

                200 First Street SW

                Rochester, MN 55905

                E‐mail: roberts.lewis@ 123456mayo.edu

                Tel.: +1‐507‐266‐4720

                or

                Bolni Marius Nagalo, Ph.D.

                Division of Hematology and Medical Oncology

                Mayo Clinic Hospital

                5777 East Mayo Boulevard

                Phoenix, AZ 85054

                E‐mail: nagalo.bolni@ 123456mayo.edu

                Tel.: +1‐480‐301‐6036

                [†]

                These authors contributed equally to this work.

                Author information
                https://orcid.org/0000-0001-8676-413X
                https://orcid.org/0000-0001-7885-8574
                Article
                HEP41595
                10.1002/hep4.1595
                7706297
                33305149
                5dfc6f7f-4635-4f05-a2e8-5e291266a616
                © 2020 The Authors. Hepatology Communications published by Wiley Periodicals LLC on behalf of the American Association for the Study of Liver Diseases.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                : 05 November 2019
                : 29 July 2020
                : 29 July 2020
                Page count
                Figures: 5, Tables: 3, Pages: 12, Words: 15289
                Funding
                Funded by: National Institute of General Medical Sciences
                Award ID: P20GM103424
                Funded by: National Cancer Institute
                Award ID: K01CA234324
                Funded by: National Institutes of Health
                Award ID: CA15083
                Award ID: CA186566
                Award ID: CA210964
                Award ID: T32 HL105355
                Award ID: TR 002377
                Award ID: UL1TR000135
                Funded by: Pietro Annigonni Biomolecular Research Center, Ouagadougou, Burkina Faso, West Africa
                Categories
                Original Article
                Original Articles
                Custom metadata
                2.0
                December 2020
                Converter:WILEY_ML3GV2_TO_JATSPMC version:5.9.4 mode:remove_FC converted:01.12.2020

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