Patients with Coexistence of Circulating Hepatitis B Surface Antigen and Its Antibody May Have a Strong Predisposition to Virus Reactivation During Immunosuppressive Therapy: A Hypothesis.
Patients with Coexistence of Circulating Hepatitis B Surface Antigen and Its Antibody May Have a Strong Predisposition to Virus Reactivation During Immunosuppressive Therapy: A Hypothesis.
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循环乙型肝炎表面抗原及其抗体共存的患者在免疫抑制治疗期间可能有很强的病毒再激活倾向:一个假设
DOI:
10.12659/msm.905033
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发表时间:
2017-12-17
期刊:
影响因子:
--
通讯作者:
Dai L
中科院分区:
文献类型:
--
作者:
Chen YL;Mo YQ;Zheng DH;Ma JD;Jing J;Dai L
Hepatitis B virus (HBV) reactivation is a well-recognized complication in patients who undergo immunosuppressive drug therapy. Although the recommendation of antiviral prophylaxis made by the American Gastroenterological Association in 2015 focuses on the risk stratification of different immunosuppressive drugs, risk factors for HBV reactivation are also worth identifying in clinical practice. Recent studies have shown that the uncommon serological pattern of coexistent circulating HBV surface antigen (HBsAg) and its antibody (anti-HBs) was associated with double mutations (A1762T/G1764A) in the basal core promoter (BCP) region of the HBV genome, which is critical for HBV replication. Here, we depicted rheumatoid arthritis (RA) patients with coexistent HBsAg and anti-HBs in our medical center, who developed HBV reactivation during immunosuppressive drug therapy. DNA sequencing analysis of the HBV genome revealed triple mutations (A1762T, G1764A, and T1753V) in the BCP region, which could further enhance the ability of HBV replication. Hence, a novel hypothesis is advanced for the first time that patients with coexistent HBsAg and anti-HBs may have a strong predisposition to HBV reactivation due to specific BCP mutations. This hypothesis would, if correct, justify the concurrent detection of HBsAg and anti-HBs in HBV screening in patients with rheumatic diseases and quickly recognize patients with high risk of HBV reactivation. Further controlled studies are needed to confirm this hypothesis.
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影响因子:
2.3
作者:
Mo YQ;Liang AQ;Ma JD;Chen LF;Zheng DH;Schumacher HR;Dai L
通讯作者:
Dai L
影响因子:
168.9
作者:
Lozano, Rafael;Naghavi, Mohsen;Murray, Christopher J. L.
通讯作者:
Murray, Christopher J. L.
影响因子:
2.7
作者:
Liu, Weiwei;Hu, Tingting;Guan, Ming
通讯作者:
Guan, Ming
影响因子:
12.7
作者:
Ding, Feng;Yu, Hong-Gang;Yu, Jie-Ping
通讯作者:
Yu, Jie-Ping
DOI:
10.1093/jnci/djp180
发表时间:
2009-08-05
期刊:
Journal of the National Cancer Institute
影响因子:
--
作者:
Liu S;Zhang H;Gu C;Yin J;He Y;Xie J;Cao G
通讯作者:
Cao G