慢性乙型肝炎患者恩替卡韦治疗期间甲胎蛋白水平依赖性早

StephenW

α-Fetoprotein level-dependent early hepatitis B surface antigen decline during entecavir therapy in chronic hepatitis B with hepatitis flare
Wen-Juei Jeng Yi-Cheng Chen Ming-Ling Chang Yun-Fan Liaw
Journal of Antimicrobial Chemotherapy, Volume 71, Issue 6, 1 June 2016, Pages 1601–1608, https://doi.org/10.1093/jac/dkw019
Published:
02 March 2016

Abstract
Objectives

Hepatitis B surface antigen (HBsAg) reduction during nucleos(t)ide analogue therapy is related to ALT level. ALT reflects hepatocytolysis while α-fetoprotein (AFP) ≥100 ng/mL during hepatitis flare reflects more extensive hepatocytolysis (bridging hepatic necrosis). The impact of AFP levels on early HBsAg kinetics during entecavir therapy was investigated.
Methods

HBsAg level was measured at baseline and months 6 and 12 of entecavir therapy in 149 chronic hepatitis B patients with hepatitis flare, defined as ALT ≥5× upper limit of normal (ULN), and 58 patients with ALT <5× ULN.
Results

There was a significantly greater HBsAg reduction in an ALT (<5, 5–10, 10–20 and ≥20× ULN, P = 0.001) and AFP (<20, 20–99 and ≥100 ng/mL, P = 0.000) level-dependent manner. In hepatitis flares with a peak AFP level ≥20 ng/mL, the differences in HBsAg reduction across all ALT levels became non-significant. HBsAg reduction was greater in genotype B- than genotype C-infected patients with baseline ALT ≥20× ULN, but the difference became non-significant in those with peak AFP ≥100 ng/mL. Multivariate linear regression analysis showed that AFP level ≥100 ng/mL, baseline HBsAg level and genotype B were independent significant factors for greater HBsAg decline at month 6 of entecavir therapy.
Conclusions

During entecavir therapy, early HBsAg reduction increased in an AFP and ALT level-dependent manner, suggesting the impact of hepatocytolysis rather than nucleos(t)ide analogue per se. Notably, a higher AFP level during hepatitis flare, reflecting more extensive hepatic necrosis, was a more powerful factor than ALT and genotype for greater HBsAg decline.

StephenW

慢性乙型肝炎患者恩替卡韦治疗期间甲胎蛋白水平依赖性早期乙型肝炎表面抗原下降
文珏耿义成陈明玲常云帆
Journal of Antimicrobial Chemotherapy，Volume 71，Issue 6,100 June 2016，Pages 1601-1608，https：//doi.org/10.1093/jac/dkw019
发布时间：
2016年3月2日

抽象
目标

核苷（酸）类似物治疗期间乙型肝炎表面抗原（HBsAg）减少与ALT水平有关。 ALT反映肝细胞溶解，而肝炎突发期间甲胎蛋白（AFP）≥100ng/ mL反映了更广泛的肝细胞溶解（桥接肝坏死）。研究了AFP水平对恩替卡韦治疗期间早期HBsAg动力学的影响。
方法

在149名患有肝炎突发的慢性乙型肝炎患者的基线和恩替卡韦治疗的第6和第12个月测量HBsAg水平，定义为ALT≥5×正常上限（ULN）和58名ALT <5×ULN的患者。
结果

ALT（<5,5-10,10-20和≥20×ULN，P = 0.001）和AFP（<20,20-99和≥100ng/ mL，P = 0.000）的HBsAg显着降低）依赖于水平的方式。在具有峰值AFP水平≥20ng/ mL的肝炎突发中，所有ALT水平的HBsAg降低的差异变得不显着。 B型基因型HBsAg降低幅度大于基线ALT≥20×ULN的基因型C型感染患者，但AFP峰值≥100ng/ mL时差异无统计学意义。多元线性回归分析显示，AFP水平≥100ng/ mL，基线HBsAg水平和基因型B是恩替卡韦治疗6个月HBsAg下降幅度较大的独立重要因素。
结论

在恩替卡韦治疗期间，早期HBsAg降低以AFP和ALT水平依赖性方式增加，表明肝细胞溶解而不是核（t）类似物本身的影响。值得注意的是，肝炎发作期间较高的AFP水平反映了更广泛的肝坏死，是一种比ALT和基因型更强的因子，可导致更大的HBsAg下降。

StephenW

https://academic.oup.com/jac/article/71/6/1601/1751338

Hepbest

核苷（酸）类似物治疗期间乙型肝炎表面抗原（HBsAg）减少与ALT水平有关
ALT良性升高和非良性升高还很难判断。
假如DNA在降低，同时ALT不超过2倍，没有硬化等症状，可以继续监控，特别不需要人为去降酶

桦子

值得注意的是，肝炎发作期间较高的AFP  水平反映了更广泛的肝坏死，是一种比ALT和基因型更强的因子，可导致更大的HBSAG  下降。
可见，这个时候HBsAG 转阴并不是好事。