Risk Factors for Long-Term Persistence of Serum Hepatitis B Surface Antigen Following Acute Hepatitis B Virus Infection in Japanese Adults
Risk Factors for Long-Term Persistence of Serum Hepatitis B Surface Antigen Following Acute Hepatitis B Virus Infection in Japanese Adults
复制标题
DOI：
10.1002/hep.26635
复制
发表时间：
2014-01-01
期刊：
影响因子：
13.5
通讯作者：
Mizokami, Masashi
中科院分区：
文献类型：
--
作者：
Ito, Kiyoaki;Yotsuyanagi, Hiroshi;Mizokami, Masashi
急性B型肝炎（AHB）后进展为慢性的患者比例在世界范围内差异很大。此外，AHB后病毒持续存在与成人B型肝炎病毒（HBV）基因型之间的关系尚不清楚。在日本进行了一项全国性的多中心研究，以评估临床和病毒学因素对AHB患者慢性结局的影响。为比较病毒持续存在的AHB患者和自限性感染患者之间的因素，在38个肝脏中心观察了212例无人类免疫缺陷病毒（HIV）合并感染的AHB患者，直至血清B肝炎表面抗原（HBsAg）消失或HBsAg持续存在的情况下至少6个月。A基因型患者HBsAg消失时间明显长于非A基因型患者。当慢性定义为HBsAg阳性持续6个月或12个月以上时，A基因型患者进展为慢性的比率较高，尽管许多由A基因型引起的病例是AHB的长期病例，而不是慢性感染。多因素logistic回归分析显示，只有基因型A与AHB后病毒持续存在独立相关。A基因型引起的AHB具有HBV DNA峰值升高和ALT峰值降低的特点。核苷酸类似物（NAs）治疗不能阻止AHB后慢性感染的进展。亚组分析表明，早期NA启动可增强病毒清除。结论：A基因型是AHB后进展为慢性感染的独立危险因素。我们的数据将有助于阐明AHB后病毒持续存在、宿主遗传因素和NAs治疗之间的相关性。（肝病学2014;58：89-97）
The proportion of patients who progress to chronicity following acute hepatitis B (AHB) varies widely worldwide. Moreover, the association between viral persistence after AHB and hepatitis B virus (HBV) genotypes in adults remains unclear. A nationwide multicenter study was conducted throughout Japan to evaluate the influence of clinical and virological factors on chronic outcomes in patients with AHB. For comparing factors between AHB patients with viral persistence and those with self-limited infection, 212 AHB patients without human immunodeficiency virus (HIV) coinfection were observed in 38 liver centers until serum hepatitis B surface antigen (HBsAg) disappeared or a minimum of 6 months in cases where HBsAg persisted. The time to disappearance of HBsAg was significantly longer for genotype A patients than that of patients infected with non-A genotypes. When chronicity was defined as the persistence of HBsAg positivity for more than 6 or 12 months, the rate of progression to chronicity was higher in patients with genotype A, although many cases caused by genotype A were prolonged cases of AHB, rather than chronic infection. Multivariate logistic regression analysis revealed only genotype A was independently associated with viral persistence following AHB. A higher peak level of HBV DNA and a lower peak of alanine aminotransferase (ALT) levels were characteristics of AHB caused by genotype A. Treatment with nucleotide analogs (NAs) did not prevent progression to chronic infection following AHB overall. Subanalysis suggested early NA initiation may enhance the viral clearance. Conclusion: Genotype A was an independent risk factor for progression to chronic infection following AHB. Our data will be useful in elucidating the association between viral persistence after AHB, host genetic factors, and treatment with NAs in future studies. (Hepatology 2014;58:89-97)