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.
J Viral Hepat. 2014 Apr;21(4):288-96. doi: 10.1111/jvh.12142. Epub 2013 Jul 30.
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.
抑制乙型肝炎病毒 (HBV)-DNA 至不可检测水平是接受抗 HBV 活性抗逆转录病毒治疗 (ART) 的 HIV/HBV 合并感染患者的重要目标，目前的指南建议在治疗 1 年内达到这一结果。然而，在临床实践中，未能在此时达到不可检测的 HBV DNA 的患者比例及其决定因素尚不清楚。本研究的目的是确定接受替诺福韦为基础的 ART 治疗 1 年后不完全 HBV 抑制的发生率和危险因素。我们对接受替诺福韦治疗的 HIV/HBV 合并感染患者进行了队列研究。患者有 HBV 病毒血症，开始接受替诺福韦为基础的 ART，并在治疗 1 年后测量 HBV DNA。主要结局是在 1 年内不完全 HBV 抑制（HBV DNA ≥2.6 log IU/mL）。逻辑回归确定了感兴趣的危险因素的不完全 HBV 抑制的比值比 (OR)。在 133 名患者中，54%（95%CI，46-63%）在 1 年内存在不完全 HBV 抑制。不完全抑制与较高的基线 HBV DNA 相关（OR，每增加 1 log IU/mL 增加 1.46；95%CI，1.1-1.94）和 1 年内可检测到的 HIV 病毒血症（OR，2.52；95%CI，1.19-5.32）。在 1 年内 HIV RNA 受抑制的 66 名患者中，28 名（42%）未能达到不可检测的 HBV DNA。相当一部分接受替诺福韦治疗的 HIV/HBV 合并感染患者在 1 年内未能抑制 HBV DNA。较高的 HBV DNA 和可检测的 HIV 病毒血症是不完全 HBV 抑制的危险因素。
