慢性乙型肝炎ALT爆发发病机制，自然病程和管理

StephenW

Journal of Hepatology

Volume 61, Issue 6, December 2014, Pages 1407–1417

Review
Hepatitis B flares in chronic hepatitis B: Pathogenesis, natural course, and management

    Ming-Ling Chang,
    Yun-Fan Liaw,


doi:10.1016/j.jhep.2014.08.033


Open Access
Summary

Hepatitis B flare, defined as an event with abrupt rise of alanine aminotransferase (ALT) levels to >5 times the upper limit of normal during chronic hepatitis B virus (HBV) infection, is considered to be the result of a human leukocyte antigen-I restricted, cytotoxic T lymphocyte mediated immune response against HBV and its downstream mechanisms. It may occur spontaneously, during or after antiviral therapy and in the setting of immunosuppression and/or chemotherapy. The clinical spectrum of hepatitis B flares varies from asymptomatic to symptomatic and typical overt acute hepatitis, even with hepatic decompensation or failure. Flares may also occur in viraemic patients with cirrhosis with higher incidence of decompensation/mortality, hence requiring immediate antiviral therapy. An upsurge of serum HBV DNA and hepatitis B surface antigen levels usually precedes the abrupt rise of ALT levels. Rising or stable and high HBV DNA during flares represent ineffective immune clearance and further hepatocytolysis, even hepatic decompensation, may occur. Such patients require immediate antiviral therapy. In contrast, bridging hepatic necrosis and/or alpha-fetoprotein levels >100 ng/ml or decreasing HBV DNA during flares represent a more effective immune clearance and frequently leads to seroclearance of HBV DNA and/or hepatitis B e antigen with remission. If patients are non-cirrhotic and there is no concern of developing decompensation, patients may be observed for 3–6 months before deciding on the need of antiviral therapy. Severe and repeated flares are prone to develop into decompensation or lead to the development of cirrhosis, thus a timely treatment to prevent the hepatitis B flare is better than to cope with the flare. Screening, monitoring and prophylactic or pre-emptive antiviral therapy is mandatory for patients who are going to receive immunosuppressants or chemotherapy.

StephenW

中华肝脏病杂志

第61卷，第6期，2014年12月，页1407至1417年

评论
发病机制，自然病程和管理：在慢性乙型肝炎耀斑

    明灵畅，
    云帆LIAW，


DOI：10.1016/ j.jhep.2014.08.033


开放存取
摘要

乙型肝炎光斑，定义为具有丙氨酸氨基转移酶的突变引起的事件（ALT）水平，以在正常过程中慢性乙型肝炎病毒（HBV）感染>5倍的上限，被认为是人类白细胞抗原Ⅰ的结果受限制，细胞毒T淋巴细胞介导的抗HBV和其下游机制的免疫应答。它可自发地发生，在此期间或抗病毒治疗后以及在免疫抑制和/或化疗的设置。乙肝耀斑的临床表现从无症状到有症状和典型的显性急性肝炎发生变化，即使肝功能失代偿或衰竭。耀斑也可发生在病毒血症肝硬化患者失代偿/死亡率的发生率较高，因此需要立即进行抗病毒治疗。的血清HBV DNA和乙型肝炎表面抗原水平的热潮一般前ALT水平的急剧上升。瑞星或在照明弹的稳定和高HBV DNA代表了无效的免疫清除，并进一步hepatocytolysis，甚至肝功能失代偿，可能会发生。这样的患者需要立即进行抗病毒治疗。与此相反，桥接肝坏死和/或甲胎蛋白水平>100毫微克/毫升或降低的HBV DNA在耀斑代表一个更有效的免疫清除并经常导致HBV-DNA的血清清除和/或乙型肝炎e抗原与缓解。如果患者无肝硬化并有发展失代偿的不关心，患者可于3-6个月决定抗病毒治疗的必要性之前观察到的。剧烈和反复的耀斑容易发展成失代偿或导致肝硬化的发展，从而及时治疗，以防止乙肝火炬优于应付光斑。筛查，监测和预防性或先发制人抗病毒治疗是必须的谁是要接受免疫抑制剂或化疗的患者。