Prevalence of HBV precore/core promoter variants in the United States

Prevalence of HBV precore/core promoter variants in the United States
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DOI:
10.1053/jhep.2003.50352
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发表时间:
2003-09-01
期刊:
影响因子:
13.5
通讯作者:
Lok, ASF
Lok, ASF
中科院分区:
医学1区
文献类型:
--
作者:
Chu, CJ;Keeffe, EB;Lok, ASF

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乙肝病毒前C区(G(1896)A)和核心启动子(A(1762)T,G(1764)A)变异可能与血清HBVDNA水平和肝病严重程度有关。这项全国性研究的目的是确定美国乙肝病毒前C/核心启动子变异的流行情况,以及这些变异与患者人口统计学、乙肝病毒基因型别、血清HBVDNA水平和肝病严重程度之间的关系。在为期一年的时间里,共有694名慢性乙肝患者在美国17个肝脏中心接受治疗。收集了人口统计学、临床和实验室数据。用线探针法检测血清中的HBV型以及前C区和C区启动子变异。用Cobas Amplicor乙肝病毒监测试剂盒检测HBVDNA定量水平。在美国,27%和44%的慢性乙肝患者中发现了前C区和核心启动子变异。在乙肝e抗原(HBeAg)阴性的患者中,前C区和核心启动子变异比HBeAg阳性的患者更常见(前C区,38%对9%;C区启动子,51%对36%;P<.001)。这些变异的流行与种族、出生地和乙肝病毒基因型有关。具有核心启动子变异的患者更有可能出现肝脏失代偿。在HBeAg阴性的患者中,前C区和/或核心启动子变异与较高的血清HBVDNA水平相关,而在HBeAg阳性的患者中则不相关。总而言之,乙肝病毒前C区和核心启动子变异在美国并不少见。医生应该意识到乙肝病毒前C区和核心启动子变异的存在,以及“HBeAg阴性慢性肝炎”的临床状况。
Variants in the precore (G(1896)A) and core promoter (A(1762)T, G(1764)A) regions of hepatitis B virus (HBV) may be related to serum HBV DNA levels and severity of liver disease. The aims of this nationwide study were to determine the prevalence of HBV precore/core promoter variants in the United States and the association between these variants and patient demographics, HBV genotypes, serum HBV DNA level, and severity of liver disease. A total of 694 consecutive chronic HBV-infected patients seen in 17 U.S. liver centers during a 1-year period were enrolled. Demographic, clinical, and laboratory data were collected. Sera were tested for HBV genotypes as well as precore and core promoter variants by line-probe assays. Quantitative HBV DNA levels were determined using Cobas Amplicor HBV Monitor kits. Precore and core promoter variants were found in 27% and 44% of patients with chronic HBV infection in the United States. Precore and core promoter variants were more common in hepatitis B e antigen (HBeAg)-negative than in HBeAg-positive patients (precore, 38% vs. 9%; core promoter, 51% vs. 36%; respectively, P < .001). The prevalence of these variants was related to ethnicity, place of birth, and HBV genotypes. Patients with core promoter variants were more likely to have hepatic decompensation. Precore and/or core promoter variants were associated with higher serum HBV DNA levels in HBeAg-negative but not in HBeAg-positive patients. In conclusion, HBV precore and core promoter variants are not rare in the United States. Physicians should be aware of the existence of HBV precore and core promoter variants and the clinical condition of "HBeAg-negative chronic hepatitis."