Wu Cheng-Kun, Chang Kuo-Chin, Hung Chao-Hung, Tseng Po-Lin, Lu Sheng-Nan, Chen Chien-Hung, Wang Jing-Houng, Lee Chuan-Mo, Tsai Ming-Chao, Lin Ming-Tsung, Yen Yi-Hao, Hu Tsung-Hui
Division of Hepato-Gastroenterology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Division of Hepato-Gastroenterology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan
J Antimicrob Chemother. 2016 Jul;71(7):1943-7. doi: 10.1093/jac/dkw097. Epub 2016 Apr 12.
Hepatitis C virus (HCV)-infected patients who achieve viral eradication may still develop hepatocellular carcinoma (HCC). Little is known about the impact of dynamic change of serum markers on HCC development.
We enrolled 1351 HCV-infected patients who achieved sustained virological response (SVR). Laboratory data were collected at least 1 year after IFN-based therapy and to the latest follow-up. Data on α-fetoprotein (AFP) were obtained >6 months prior to HCC development to exclude HCC-related AFP elevation.
HCC developed in 49 patients. Risk factors for HCC in SVR patients were old age, liver cirrhosis, higher pre- and post-treatment AFP and high post-treatment AST-to-platelet ratio index (APRI). Patients with pre-AFP ≥15 ng/mL → post-AFP ≥15 ng/mL (at 1 year, 23.1%; 5 years, 42.3%) and pre-AFP <15 ng/mL → post-AFP ≥15 ng/mL (at 1 year, 25%; 5 years, 50%) had the highest risk of HCC development, followed by pre-AFP ≥15 ng/mL → post-AFP <15 ng/mL (at 1 year, 5.2%; 5 years, 7.6%) and pre-AFP <15 ng/mL → post-AFP ng/mL <15 ng/mL (at 1 year, 0.5%; 5 years, 0.9%) (P < 0.001). The pattern was similar for platelets and APRI (P < 0.001). SVR patients with pre-APRI ≥0.7 → post-APRI ≥0.7 had the highest risk of HCC development, followed by comparable risks among the other three groups.
SVR patients with a persistently high AFP level (≥15 ng/mL) and a high APRI (≥0.7) before and after treatment had the highest incidence of HCC development. Patients with a reduction of AFP and APRI to the normal range after treatment had a markedly decreased risk of HCC. The risk was lowest for patients who kept persistently normal AFP and APRI before and after treatment.
实现病毒清除的丙型肝炎病毒(HCV)感染患者仍可能发生肝细胞癌(HCC)。关于血清标志物动态变化对HCC发生的影响知之甚少。
我们纳入了1351例实现持续病毒学应答(SVR)的HCV感染患者。在基于干扰素的治疗后至少1年及最新随访时收集实验室数据。甲胎蛋白(AFP)数据在HCC发生前>6个月获得,以排除与HCC相关的AFP升高。
49例患者发生了HCC。SVR患者发生HCC的危险因素为老年、肝硬化、治疗前后较高的AFP以及治疗后较高的AST与血小板比值指数(APRI)。治疗前AFP≥15 ng/mL→治疗后AFP≥15 ng/mL(1年时为23.1%;5年时为42.3%)以及治疗前AFP<15 ng/mL→治疗后AFP≥15 ng/mL(1年时为25%;5年时为50%)的患者发生HCC的风险最高,其次是治疗前AFP≥15 ng/mL→治疗后AFP<15 ng/mL(1年时为5.2%;5年时为7.6%)以及治疗前AFP<15 ng/mL→治疗后AFP<15 ng/mL(1年时为0.5%;5年时为0.9%)(P<0.001)。血小板和APRI的模式相似(P<0.001)。治疗前APRI≥0.7→治疗后APRI≥0.7的SVR患者发生HCC的风险最高,其次是其他三组风险相当。
治疗前后AFP水平持续较高(≥15 ng/mL)且APRI较高(≥0.7)的SVR患者发生HCC的发生率最高。治疗后AFP和APRI降至正常范围的患者发生HCC的风险显著降低。治疗前后AFP和APRI持续正常的患者风险最低。