首页> 外文期刊>Antiviral therapy >Hepatitis B surface antigen (HBsAg) decrease and serum interferon-inducible protein-10 levels as predictive markers for HBsAg loss during treatment with nucleosideucleotide analogues.
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Hepatitis B surface antigen (HBsAg) decrease and serum interferon-inducible protein-10 levels as predictive markers for HBsAg loss during treatment with nucleosideucleotide analogues.

机译:乙型肝炎表面抗原(HBsAg)降低和血清干扰素诱导型蛋白10水平可作为用核苷/核苷酸类似物治疗期间HBsAg丢失的预测标志物。

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BACKGROUND: Hepatitis B surface antigen (HBsAg) loss is the ultimate goal of antiviral therapy and its prediction may be important for treatment individualization. Quantitative HBsAg (qHBsAg) has been shown to predict response to interferon-alpha, but few studies have analysed qHBsAg during treatment with nucleosideucleotide analogues (NAs). Serum interferon-inducible protein-10 (IP-10) has been associated with treatment response in hepatitis C, but data in chronic hepatitis B are lacking. Here, we aimed to investigate potential factors predictive for HBsAg loss. METHODS: HBsAg was quantified at multiple time points in 126 patients with chronic HBV infection; 95 received NA treatment for 6-107 months. At an early time point (first 6 months of therapy) and late time point after virological response (VR; HBV DNA<100 IU/ml), we distinguished three patterns of HBsAg decrease: strong decrease (>0.5 log(10)), moderate decrease (10% to 0.5 log(10)) and no decrease (<10%). In addition to conventional biochemical and virological parameters, we analysed serum IP-10 levels in 55 patients. RESULTS: Early and late HBsAg kinetics did not correlate. Overall, 42% of patients with a strong HBsAg decrease 2 years after VR cleared HBsAg. Importantly, no patient without a late HBsAg decrease >0.5 log(10) cleared HBsAg. By contrast, early HBsAg decrease after 6 months of NA therapy was not associated with HBsAg loss. Baseline serum IP-10 levels were associated with late but not early HBsAg kinetics and were highest in patients with HBsAg loss. CONCLUSIONS: Monitoring qHBsAg after successful HBV DNA suppression might be useful to identify patients who clear HBsAg, implicating finite NA treatment. The role of IP-10 as predictive marker for HBsAg loss should be further evaluated.
机译:背景:乙型肝炎表面抗原(HBsAg)的丢失是抗病毒治疗的最终目标,其预测对个体化治疗可能很重要。定量HBsAg(qHBsAg)已显示出可预测对干扰素-α的反应,但很少有研究在用核苷/核苷酸类似物(NAs)治疗期间分析qHBsAg。血清干扰素诱导蛋白-10(IP-10)与丙型肝炎的治疗反应有关,但缺乏慢性乙型肝炎的数据。在这里,我们旨在调查可预测HBsAg丢失的潜在因素。方法:对126例慢性HBV感染患者在多个时间点进行HBsAg定量分析。 95例接受了NA治疗6-107个月。在病毒学应答的早期时间点(治疗的前6个月)和病毒学应答后的晚期时间点(VR; HBV DNA <100 IU / ml),我们区分了HBsAg降低的三种模式:强烈降低(> 0.5 log(10)),适度下降(10%至0.5 log(10)),而没有下降(<10%)。除了常规的生化和病毒学参数外,我们还分析了55例患者的血清IP-10水平。结果:早期和晚期HBsAg动力学无相关性。总体而言,VR清除HBsAg后2年,有HBsAg强的患者减少了42%。重要的是,没有晚期HBsAg下降> 0.5 log(10)的患者不会清除HBsAg。相比之下,NA治疗6个月后早期HBsAg降低与HBsAg丢失无关。基线血清IP-10水平与晚期而非早期HBsAg动力学相关,在HBsAg丧失的患者中最高。结论:成功抑制HBV DNA后监测qHBsAg可能有助于识别清除HBsAg的患者,这意味着需要进行有限的NA治疗。 IP-10作为HBsAg丢失的预测指标的作用应进一步评估。

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