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-coinfected patients receiving anti-HBV-active antiretroviral therapy (ART), and current guidelines recommend that this outcome should be reached by one 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 one year of tenofovir-based ART. We performed a cohort study among tenofovir-treated HIV/HBV-coinfected patients. Patients had HBV viremia, initiated tenofovir-based ART, and had HBV DNA measured at one year of therapy. The primary outcome was incomplete HBV suppression (HBV DNA ≥2.6 log IU/mL) at one 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 one 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 viremia at one year (OR, 2.52; 95% CI, 1.19–5.32). Among 66 patients with suppressed HIV RNA at one year, 28 (42%) failed to achieve an undetectable HBV DNA. Failure to suppress HBV DNA by one year occurred in a sizeable proportion of tenofovir-treated HIV/HBV-coinfected patients. Higher HBV DNA and detectable HIV viremia were risk factors for incomplete HBV suppression.

Impact of Antiretroviral Therapy on Liver Fibrosis Among Human Immunodeficiency Virus-Infected Adults With and Without HBV Coinfection in Zambia

“…Our finding that two-thirds of patients achieved HBV VS by 1 year is similar to findings from another study in the region and 1 in the United States [28,29]. Longer follow-up of HBV VL may be needed to document full HBV VS.…”

“…Although it was not observed in our study, HIV VS, another marker of adherence, predicted HBV VS among 133 HIV-HBV patients on TDF-containing ART in the United States [29]. The rate of HBsAg loss (12.1%) we observed was higher than what has been listed in many reports from HIV-HBV-coinfected and CHB patients in high-income countries [32][33][34] but similar to the 17.6% reported by Hamers et al [29] and lower than the 36% observed by Anderson et al [35]. Our rate of HBsAg loss may be slightly overestimated due to our use of a rapid test on whole blood that has lower sensitivity than serum assays [36].…”

HBV Genotypes and Drug Resistance Mutations in Antiretroviral Treatment-Naive and Treatment-Experienced HBV–HIV-Coinfected Patients

“…HIV co-infection is a major cause of morbidity and mortality of HBV infection as it is associated with an increased risk of progression to liver cirrhosis and HCC [3]. Effective antiviral therapy is indicated to reduce the viral replication and risk of HBV progression [4]. Major advancements in the treatment of chronic HBV have been made during the last decade with the development of nucleoside reverse transcriptase inhibitors (NRTIs) with anti-HBV activity such as L-nucleosides (lamivudine (3TC) and telbivudine), alkyl phosphonates (adefovir dipivoxil and tenofovir disoproxil fumarate), or D-cyclopentanes (entecavir) [7].…”

Risk of End-Stage Liver Disease in HIV-Viral Hepatitis Coinfected Persons in North America From the Early to Modern Antiretroviral Therapy Eras

“…HBV therapy also may not be fully effective in the setting of HIV. A large proportion of HIV/HBV-coinfected patients fail to achieve HBV DNA suppression despite use of TDF-based ART [35,36]. In coinfected patients with prior 3TC experience receiving TDF and FTC/ 3TC, HBV DNA was detected in 20% of follow-up visits over 2 years [37].…”