Relationship between HBsAg, HBcrAg and hepatocellular carcinoma in patients with undetectable HBV DNA under nucleos(t)ide therapy
Relationship between HBsAg, HBcrAg and hepatocellular carcinoma in patients with undetectable HBV DNA under nucleos(t)ide therapy
复制标题
DOI：
10.1111/jvh.12688
复制
发表时间：
2017-08-01
影响因子：
2.5
通讯作者：
Yuen, M. -F.
中科院分区：
文献类型：
--
作者：
Cheung, K. -S.;Seto, W. -K.;Yuen, M. -F.
我们研究了在接受核苷类似物（NA）的血清HBV DNA检测不出的患者中，乙型肝炎表面和核心相关抗原（HBsAg, HBcrAg）与肝细胞癌（HCC）发展之间的关系。76名HBV DNA检测不出（< 20 IU/mL）的HBV携带者随后发展为HCC，与152名匹配的对照组进行比较。分析了临床和实验室参数（包括测量线性化HBsAg [HQ-HBsAg]和HBcrAg的新检测方法）。两组患者HBsAg/HQ-HBsAg水平差异无统计学意义。HCC组和对照组na前和na后HBcrAg水平中位数差异有统计学意义(治疗前：279.0 vs 35.4 kU/mL， P=。005年;处理后：10.2 vs 1.7 kU/mL， P=。005年,分别)。对于整个HCC组，治疗后HBcrAg水平的临界值为7.8 kU/mL，受试者工作曲线下面积（AUROC）为0.61，阴性预测值（NPV）为77.0%。HCC发展的OR为3.27。对于非肝硬化患者，HCC组和对照组治疗后HBcrAg水平的中位数分别为10.2和1.0 kU/mL （P= 0.05）。001)。当HBcrAg水平为7.9 kU/mL时，AUROC为0.70，NPV为80.6%。HCC发展的OR为5.95。在接受NA治疗时血清HBV DNA检测不到的患者中，较高的NA治疗前后HBcrAg水平（而非HBsAg）与HCC发展风险增加相关。在这组患者中，HBcrAg可能作为一种新的HCC风险标志物。
We examined the relationship between hepatitis B surface and core-related antigens (HBsAg, HBcrAg) and hepatocellular carcinoma (HCC) development in patients with undetectable serum HBV DNA receiving nucleos(t)ide analogue (NA). Seventy-six HBV carriers with undetectable HBV DNA (< 20 IU/mL) who subsequently developed HCC were compared with 152 matched controls. Clinical and laboratory parameters (including novel assays to measure linearized HBsAg [HQ-HBsAg] and HBcrAg) were analysed. There were no significant differences in HBsAg/HQ-HBsAg levels between the two groups. There was a significant difference in the median values of both pre-and post-NA HBcrAg levels between the HCC and control groups (pre-treatment: 279.0 vs 35.4 kU/mL, P=. 005; post-treatment: 10.2 vs 1.7 kU/mL, P=. 005, respectively). For the whole HCC group, a cut-off value of post-treatment HBcrAg level = 7.8 kU/mL yielded an area under receiver operating curve (AUROC) of 0.61 with a negative predictive value (NPV) of 77.0%. The OR of HCC development was 3.27. For noncirrhotic patients, the median values of post--treatment HBcrAg level of HCC group and controls were 10.2 and 1.0 kU/mL, respectively (P=. 001). A cut-off value of HBcrAg level = 7.9 kU/mL yielded an AUROC of 0.70 with a NPV of 80.6%. The OR of HCC development was 5.95. A higher pre- and post-NA treatment HBcrAg level (but not HBsAg) was associated with an increased risk of HCC development in patients achieving undetectable serum HBV DNA while on NA therapy. HBcrAg may serve as a novel risk marker for HCC in this group of patients.