抗病毒治疗期间或之后Hbsag损失的持久性及其对临床结果的影响

G. Teuber
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摘要

目的:关于在抗病毒治疗期间或之后HBsAg损失的持久性,只有少数研究结果相互矛盾,表明HBsAg和/或HBV-DNA复发的再激活率为4.2%(16.4%),主要是亚洲患者。然而,目前欧洲还没有更大规模的关于乙肝表面抗原在抗病毒治疗期间或之后损失的持久性以及对进一步临床结果的影响的研究。患者和方法:在这项回顾性的德国多中心研究中,纳入了143例在抗病毒治疗期间或治疗后HBsAg丢失的慢性乙型肝炎患者(平均年龄:43±13.8岁,男性93例,女性50例)。2008年4月至2014年7月期间,使用聚乙二醇干扰素- α 2a (PegIFNalpha2a)和/或核苷进行抗病毒治疗。在抗病毒治疗前,17例患者已建立肝硬化。主要终点是HBsAg再激活,进一步的终点是临床进展性肝病、肝移植和死亡。结果:在随访期间(平均3.0±2.1年),仅有3/143例患者(2.1%)出现HBsAg复发,且无既往血清转化为Anti-HBs的患者。这些患者的HBV再激活与可检测到的HBV- dna水平无关,2/3的患者基线肝硬化,1/2的患者随后死于复发性多灶性肝细胞癌。在140例持续HBsAg丢失的患者中,2例最初肝硬化患者死亡,1例接受肝移植,均因肝细胞癌。结论:在以白人为主的患者群体中,在抗病毒治疗期间和/或之后HBsAg的损失似乎是持久的,再激活率低。然而,肝硬化患者发生肝细胞癌的风险很高,即使在HBsAg消失后也是如此。对这些患者的持续监测似乎是强制性的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Durability of Hbsag Loss During or After Antiviral Treatment and Impact on Clinical Outcome
Aims: Concerning the durability of HBsAg loss during or after antiviral treatment only a few studies with conflicting results are available indicating a rate of reactivation with reocurrence of HBsAg and/or HBV-DNA in 4.2% 16.4% in predominantly Asian patients. However, there are no larger European studies available concerning the durability of HBsAg loss during or after antiviral treatment and the impact on further clinical outcome. Patients and Methods: In this retrospective German multicentre study, 143 patients with chronic hepatitis B (mean age: 43 ± 13.8 years, 93 males, 50 females) who lost HBsAg during or after antiviral treatment were included. Antiviral treatment with peginterferon-alpha2a (PegIFNalpha2a) and/or nucleus(t)ides were administered between April 2008 and July 2014. Before antiviral treatment, 17 patients had established liver cirrhosis. Primary endpoint was reactivation with reoccurrence of HBsAg Further endpoints were clinical progressive liver disease, liver transplantation and death. Result: During the follow-up period (mean: 3.0 ± 2.1 years) a reoccurrence of HBsAg was observed in only 3/143 patients (2.1%), and in none with previous seroconversion to Anti-HBs. The HBV reactivation in these patients was not associated with detectable HBV-DNA levels, 2/3 patients had baseline cirrhosis and 1/2 subsequently died due to recurrent multifocal hepatocellular carcinoma. Among the 140 patients with persisting HBsAg loss, two initially cirrhotic patients died, and one received liver transplantation all due to hepatocellular carcinoma. Conclusion: In a predominantly Caucasian patient population HBsAg loss during and/or after antiviral treatment seems to be durable with low rates of reactivation. Cirrhotic patients, however, have a high risk developing hepatocellular carcinoma even after HBsAg loss. Continous surveillance in these patients seems to be mandatory.
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