e抗原阴性和D基因型乙肝患者治疗过程中的HBsAg动力学和转阴

StephenW

http://www.docguide.com/kinetics-and-prediction-hbsag-loss-during-therapy-analogues-patients-affected-chronic-hepatitis-b-hb?hash=c8431e6c&eid=30702&alrhash=2f4244-e14fac0ff7ef1d5b0c78458126191858
Source: Liver Int  |  Posted 6 days ago
Kinetics and prediction of HBsAg loss during therapy with analogues in patients affected by chronic hepatitis B HBeAg negative and genotype D;
Boglione L, D'Avolio A, Cariti G, Gregori G, Burdino E, Baietto L, Cusato J, Ghisetti V, De Rosa FG, Perri GD; Liver International (Dec 2012)


BACKGROUND AND AIMS: In patients affected by chronic hepatitis because of HBV infection, long-term suppressive therapy with nucleos(t)ides analogues in the HBeAg- patients has shown low effects on HBsAg titre (qHBsAg) decrease, and HBsAg loss is difficult to achieve. Thus, in this type of patients the main goals of antiviral therapy is the suppression of HBV-DNA and ALT normalization. METHODS: We retrospectively evaluated different qHBsAg kinetics in 134 treatment-naïve patients having the same characteristics: HBeAg-, infection sustained by HBV genotype D and persistently undetectable HBV-DNA. Patients were treated with NAs therapy (lamivudine, adefovir, telbivudine, entecavir and tenofovir) for at least 2 years. qHBsAg was performed every 6 months. RESULTS: Our results showed a significantly greater qHBsAg decline after 2 years in patients treated with tenofovir (0.45 logIU/ml) than in patients treated with telbivudine (0.12 logIU/ml; P < 0.001). The calculated expected time to HBsAg loss was shorter in the tenofovir group than in the telbivudine group (nearly 17 vs 63 years, P < 0.001). CONCLUSIONS: HBeAg negative patients infected by HBV genotype D should be treated with more potent NAs such as entecavir or tenofovir to obtain a significant qHBsAg decrease, but the achievement of HBsAg loss seems to require almost two decades of therapy.

StephenW

背景与目的：因为HBV感染者，长期抑制治疗的核苷（酸）的IDE类似物的患者e抗原慢性肝炎患者的影响，对HBsAg滴度（qHBsAg）的减少，显示出低的影响及乙型肝炎病毒表面抗原损失是难以实现的。因此，在这种类型的患者进行抗病毒治疗的主要目标是抑制的HBV-DNA和ALT正常化。方法：我们回顾性分析不同qHBsAg动力学在134治疗初治患者具有相同的特点：e抗原，持续感染HBV基因型D和持续检测不到HBV-DNA。患者接受治疗与NAS（拉米夫定，阿德福韦，替比夫定，恩替卡韦和替诺福韦）治疗至少2年。 qHBsAg进行每6个月。结果：我们的研究结果显示，2年后下降显着更大的qHBsAg在替诺福韦时（0.45 logIU/毫升）比替比夫定治疗的患者（0.12 logIU/毫升，P <0.001）治疗的患者中。计算出的预期HBsAg消失的时间短，替诺福韦组在替比夫定组（近17 VS63岁，P <0.001）。结论：HBeAg阴性患者HBV基因型D感染，应被视为与更有效的NAS，如恩替卡韦或替诺福韦获得显著qHBsAg的下降，但实现的HBsAg转阴似乎需要近二十年的治疗。

sddp1

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能抚平精神与肉体病痛的，似乎只有时间

StephenW

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干扰素可以缩短这个时间. 此外，长期使用抗病毒药物可以复原我们抗-HBV的免疫.

sddp1

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虽然有些缩短，但是仍然很漫长。不过谢谢斯蒂文给我们带来的新鲜空气

StephenW

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目前结合PEGIFN+ NUCs治疗理论 (何时以及如何尚不清楚).
Fig. 1. Combination therapy may lead to restoration of both arms of the immune system, NK cells (top row) as well as CD8+ T cells (middle row), that are typically
dysfunctional during chronic HBV infection and only partially restored by either therapy. Effects on human hepatocytes are shown in the bottom row: after cccDNAdriven
transcription of the viral RNAs, the pregenomic RNA (pgRNA) is encapsidated and reverse transcribed by the HBV polymerase. Through Golgi and endoplasmatic
reticulum the core particles acquire the envelope and are secreted. Transcription of the subgenomic HBV-RNAs leads to the production of the envelope proteins, which are
needed for virion secretion and to produce the non-infectious subviral particles (SVPs). While NUCs therapy efficiently suppresses HBV replication, IFN administration can
also suppress cccDNA transcription and hence viral antigen production.
图。 1。联合治疗可能导致免疫系统的细胞，NK细胞（顶行）及CD8+ T细胞（中间行）的两个臂的恢复，即通常
不正常的慢性HBV感染过程中，仅部分恢复或者治疗。对人类肝细胞的影响显示在底行：cccDNAdriven后
病毒RNA的转录，前基因组RNA（pgRNA），被包被的HBV聚合酶和反转录。通过高尔基体和内质
网的核心颗粒获得的信封和分泌。亚基因组HBV-的RNA的转录导致的包膜蛋白的生产，这是
所需的病毒颗粒的分泌，并产生非感染性的亚病毒颗粒（SVP的）。虽然NUCs治疗有效地抑制HBV复制，IFN管理
也cccDNA的转录，从而抑制病毒抗原生产.