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J Acquir Immune Defic Syndr. 2016 Jul 1;72(3):274-80. doi: 10.1097/QAI.0000000000000969.

Isolated Hepatitis B Core Antibody Status Is Not Associated With Accelerated Liver Disease Progression in HIV/Hepatitis C Coinfection.

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*CORE Center/Stroger Hospital of Cook County, Chicago, IL; †Department of Medicine, Rush University Medical Center, Chicago, IL; ‡Department of Medicine, Georgetown University Medical Center, Washington, DC; §Department of Medicine, University of Southern California Keck School of Medicine, Los Angeles, CA; ‖Department of Medicine, State University of New York, Downstate, Brooklyn, NY; ¶Department of Medicine, Montefiore Medical Center, Bronx, NY; #Johns Hopkins Bloomberg School of Public Health, Baltimore, MD; **Institute for Liver and Digestive Health, Division of Medicine, University College London, London, United Kingdom; and ††Department of Medicine, University of California San Francisco, San Francisco, CA.



Isolated hepatitis B core antibody (anti-HBc) is a common serologic finding in HIV-infected persons, but the clinical significance is uncertain. We studied HIV/hepatitis C virus (HCV)-infected women over time to determine whether the trajectory of liver disease progression is affected by isolated anti-HBc serologic status.


We performed serial enhanced liver fibrosis (ELF) markers on HIV/HCV-coinfected women to assess liver disease progression trajectory over time comparing women with isolated anti-HBc to women with either negative HB serologies, anti-HBs alone, or anti-HBc and anti-HBs. ELF, a serum marker that combines direct markers of extracellular matrix remodeling and fibrosis, was performed on serum stored biannually. Women with at least 3 ELF determinations and persistent HCV RNA positivity were included.


Three hundred forty-four women, including 132 with isolated anti-HBc and 212 with other serologic findings, were included. A median of 6 (interquartile range, 5-7) biannual ELF values was available for each woman, totaling 2119 visits. ELF increased over time from a median of 9.07 for women with isolated anti-HBc and 9.10 for those without isolated anti-HBc to 9.83 and 9.88, respectively, with no difference in degree of change or slope in the mixed-effects model including age, race, CD4 count, antiretroviral therapy, and drug and alcohol use. Factors independently associated with liver disease progression were older age, lower CD4, antiretroviral therapy nonuse, and Hispanic ethnicity.


Isolated anti-HBc serologic status was not associated with accelerated liver disease progression over a median of 9.5 years among HIV/HCV-coinfected women.

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