Department of General Internal Medicine 2, Kawasaki Hospital, Kawasaki Medical School, Okayama, Japan.
Department of Gastroenterology and Hepatology, Kinki University School of Medicine, Osaka, Japan.
Liver Cancer. 2014 Mar;3(1):41-52. doi: 10.1159/000343857.
Serum levels of hepatitis B virus (HBV) DNA are an important predictor of the risk of hepatocellular carcinoma (HCC) in patients with chronic HBV infection. However, little is known about whether high levels of hepatitis B surface antigen (HBsAg) increase the risk for HCC.
We investigated 167 patients who were treated with nucleos(t)ide analogues (NA) for at least 2 years (median: 5.8 years, range: 2-13.1 years). Relationships between reduced levels of HBsAg and various factors were evaluated. In addition, we evaluated the usefulness of quantitative serum levels of HBV DNA and HBsAg as predictors of HCC development in patients receiving long-term NA therapy.
HCC developed in 9 of the 167 NA-treated patients. In the 9 patients with HCC, HBV DNA was undetectable (<2.1 log copies/mL), but HBsAg levels were ≥2000 C.O.I. in 7 patients. No maternal transmission, long NA treatment period, HBV DNA levels <3.0 log copies/mL, and reduced hepatitis B e antigen levels during the first 24 weeks of treatment were a significant factor of HBsAg levels <2000 C.O.I..
Hepatocarcinogenesis was observed in patients with high HBsAg levels, despite the negative conversion of HBV DNA as a result of long-term NA therapy. Therefore, to suppress hepatocarcinogenesis, it is important to control not only HBV DNA levels but also HBsAg levels.
血清乙型肝炎病毒（HBV）DNA 水平是慢性 HBV 感染患者发生肝细胞癌（HCC）风险的重要预测指标。然而，HBsAg 水平升高是否会增加 HCC 风险知之甚少。
我们研究了 167 例至少接受核苷（酸）类似物（NA）治疗 2 年以上（中位数：5.8 年，范围：2-13.1 年）的患者。评估了 HBsAg 水平降低与各种因素的关系。此外，我们评估了定量血清 HBV DNA 和 HBsAg 水平作为预测长期 NA 治疗患者 HCC 发展的有用性。
9 例 NA 治疗患者发生 HCC。在 9 例 HCC 患者中，HBV DNA 不可检测（<2.1 log 拷贝/mL），但 7 例患者 HBsAg 水平≥2000 C.O.I.。无母婴传播、NA 治疗时间长、HBV DNA 水平<3.0 log 拷贝/mL、治疗前 24 周 HBeAg 水平降低是 HBsAg 水平<2000 C.O.I.的显著因素。
尽管长期 NA 治疗导致 HBV DNA 转阴，但仍观察到高 HBsAg 水平患者发生肝癌。因此，为了抑制肝癌发生，不仅要控制 HBV DNA 水平，还要控制 HBsAg 水平。
