title: Incidence and risk factors for incomplete HBV DNA suppression in HIV/HBV-co-infected patients initiating tenofovir-based therapy.
abstract: Suppression of hepatitis B virus (HBV)-DNA to undetectable levels is an important goal for HIV/HBV-co-infected patients receiving anti-HBV-active antiretroviral therapy (ART), and current guidelines recommend that this outcome should be reached by 1 year of treatment. However, the proportion of patients that fail to achieve an undetectable HBV DNA at this time point and its determinants remain unknown in clinical practice. The objective of this study was to determine the incidence and risk factors for incomplete HBV suppression following 1 year of tenofovir-based ART. We performed a cohort study among tenofovir-treated HIV/HBV-co-infected patients. Patients had HBV viraemia, initiated tenofovir-based ART and had HBV DNA measured at 1 year of therapy. The primary outcome was incomplete HBV suppression (HBV DNA ≥2.6 log IU/mL) at 1 year. Logistic regression determined odds ratio (ORs) of incomplete HBV suppression for risk factors of interest. Among 133 patients, 54% (95% CI, 46-63%) had incomplete HBV suppression at 1 year. Incomplete suppression was associated with higher baseline HBV DNA (OR, 1.46 per log IU/mL increase; 95% CI, 1.1-1.94) and detectable HIV viraemia at 1 year (OR, 2.52; 95% CI, 1.19-5.32). Among 66 patients with suppressed HIV RNA at 1 year, 28 (42%) failed to achieve an undetectable HBV DNA. Failure to suppress HBV DNA by 1 year occurred in a sizeable proportion of tenofovir-treated HIV/HBV-co-infected patients. Higher HBV DNA and detectable HIV viraemia were risk factors for incomplete HBV suppression.
authors.affiliation: Division of Infectious Diseases, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA; Department of Biostatistics and Epidemiology, Center for Clinical Epidemiology and Biostatistics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA; Medicine Service, Philadelphia Veterans Affairs Medical Center, Philadelphia, PA, USA.
authors.forename: J S
authors.initials: JS
authors.lastname: Hafkin
authors.forename: M K
authors.initials: MK
authors.lastname: Osborn
authors.forename: A R
authors.initials: AR
authors.lastname: Localio
authors.forename: V K
authors.initials: VK
authors.lastname: Amorosa
authors.forename: J R
authors.initials: JR
authors.lastname: Kostman
authors.forename: J J
authors.initials: JJ
authors.lastname: Stern
authors.forename: P
authors.initials: P
authors.lastname: De La Torre
authors.forename: K
authors.initials: K
authors.lastname: Mounzer
authors.forename: I
authors.initials: I
authors.lastname: Frank
authors.forename: R
authors.initials: R
authors.lastname: Gross
authors.forename: K-M
authors.initials: KM
authors.lastname: Chang
authors.forename: V
authors.initials: V
authors.lastname: Lo Re
mesh_terms: D000225:Adenine / Q000031:analogs & derivatives / Q000627:therapeutic use; D000328:Adult; D019380:Anti-HIV Agents / Q000627:therapeutic use*; D023241:Antiretroviral Therapy, Highly Active; D015331:Cohort Studies; D060085:Coinfection; D004279:DNA, Viral / Q000097:blood*; D024882:Drug Resistance, Viral; D005260:Female; D015658:HIV Infections / Q000150:complications / Q000188:drug therapy* / Q000821:virology; D006509:Hepatitis B / Q000150:complications / Q000188:drug therapy* / Q000821:virology; D006515:Hepatitis B virus / Q000235:genetics / Q000502:physiology*; D006801:Humans; D015994:Incidence; D019259:Lamivudine / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D063065:Organophosphonates / Q000627:therapeutic use; D012189:Retrospective Studies; D012307:Risk Factors; D000068698:Tenofovir; D019562:Viral Load; D014766:Viremia
chemical_list: D019380:Anti-HIV Agents; D004279:DNA, Viral; D063065:Organophosphonates; D019259:Lamivudine; D000068698:Tenofovir; D000225:Adenine
keywords: HIV; HIV/hepatitis B virus co-infection; hepatitis B virus; lamivudine; tenofovir