改善慢性乙型肝炎病毒感染的临床结局

StephenW

Improving clinical outcomes of chronic hepatitis B virus infection
Tung-Hung Su & Jia-Horng Kao
Pages 141-154 | Published online: 22 Sep 2014

    Download citation https://doi.org/10.1586/17474124.2015.960398 CrossMark Logo CrossMark

Abstract

Chronic hepatitis B virus (HBV) infection is a global health problem, leading to cirrhosis, hepatocellular carcinoma (HCC) and liver-related deaths. Universal hepatitis B vaccination is the most cost–effective way to eradicate HBV infection with the remarkable reduction of chronic carriage, neonatal fulminant hepatitis and childhood HCC. The introduction of highly effective antiviral agents, including lamivudine, adefovir dipivoxil, entecavir, telbivudine, tenofovir disoproxil fumarate and pegylated interferons further improve short-, medium- and long-term outcomes of chronic HBV infection, such as ALT normalization, HBV DNA suppression, HBeAg seroconversion, HBsAg seroclearance, fibrosis regression, reduction of cirrhosis, HCC, liver-related deaths and the need for liver transplantation. Above all, sustained and profound viral suppression is the key to improve the clinical outcomes of chronic hepatitis B.

Keywords: adefovir dipivoxil cirrhosis entecavir hepatocellular carcinoma interferon lamivudine liver transplantation telbivudine tenofovir disoproxil fumarate vaccination

Key issues

    The universal hepatitis B virus (HBV) vaccination markedly decreases chronic hepatitis B surface antigen (HBsAg) carriage, neonatal fulminant hepatitis and childhood hepatocellular carcinoma (HCC).

    The short-term therapeutic goals including alanine aminotransferase normalization, HBV viral suppression, HBeAg loss/seroconversion and histologic improvement continue to improve after extending antiviral therapy with maintained viral suppression.

    Serum quantitative HBsAg titer reflects the active transcription of covalently closed circular DNA in hepatocyte and its clearance is close to the cure of chronic hepatitis B.

    Regression of liver fibrosis after prolonged antiviral therapy with maintained viral suppression is possible.

    Successful pegylated interferons or nucleos(t)ide analog therapy can halt disease progression and delay or prevent the development of cirrhosis and its complications.

    Compared with untreated controls, long-term NA therapy can reduce the development of HCC, especially in compensated cirrhotic patients, but not in decompensated ones.

    Despite the reduction of HCC risk after NA therapy, periodic HCC surveillance is still recommended in high-risk patients.

    Safety profiles of prolonged NA therapy is a growing concern, and renal function, bone mineral density should be monitored regularly.

StephenW

改善慢性乙型肝炎病毒感染的临床结局
苏东雄＆高佳鸿
第141-154页|在线发布：2014年9月22日

    下载引文https://doi.org/10.1586/17474124.2015.960398 CrossMark徽标CrossMark

抽象的

慢性乙型肝炎病毒（HBV）感染是全球性的健康问题，导致肝硬化，肝细胞癌（HCC）和与肝有关的死亡。普遍接种乙型肝炎疫苗是消除乙肝病毒感染的最经济有效的方法，它可以显着减少慢性病携带，新生儿暴发性肝炎和儿童期HCC。引入高效抗病毒剂，包括拉米夫定，阿德福韦酯，恩替卡韦，替比夫定，替诺福韦富马酸替诺福韦酯和聚乙二醇化干扰素，进一步改善了慢性HBV感染的短期，中期和长期结果，例如ALT正常化，HBV DNA抑制， HBeAg血清转化，HBsAg血清清除，纤维化消退，肝硬化减少，HCC，肝相关死亡以及需要肝移植。最重要的是，持续而深刻的病毒抑制是改善慢性乙型肝炎临床疗效的关键。

关键词：阿德福韦酯乙肝硬化恩替卡韦肝细胞癌干扰素拉米夫定肝移植替比夫定替诺福韦替莫索尔富马酸盐疫苗接种

关键问题

    通用乙型肝炎病毒（HBV）疫苗接种可显着减少慢性乙型肝炎表面抗原（HBsAg）携带，新生儿暴发性肝炎和儿童肝细胞癌（HCC）。

    延长抗病毒治疗并维持病毒抑制后，包括丙氨酸转氨酶正常化，HBV病毒抑制，HBeAg丢失/血清转化和组织学改善在内的短期治疗目标将继续改善。

    血清定量HBsAg滴度反映了肝细胞中共价闭合环状DNA的活跃转录，其清除率接近于慢性乙型肝炎的治愈。

    长时间抗病毒治疗并保持病毒抑制后，肝纤维化可能会消退。

    成功的聚乙二醇化干扰素或核苷类似物疗法可以阻止疾病进展并延缓或预防肝硬化及其并发症的发展。

    与未经治疗的对照组相比，长期NA治疗可以减少HCC的发展，尤其是在代偿性肝硬化患者中，而在代偿失调的患者中则不能。

    尽管NA治疗后降低了HCC风险，但仍建议在高危患者中定期进行HCC监测。

    长期NA治疗的安全性问题日益引起人们的关注，应定期监测肾功能，骨矿物质密度。