Yoo S H, Kwon J H, Nam S W, Kim H Y, Kim C W, You C R, Choi S W, Cho S H, Han J-Y, Song D S, Chang U I, Yang J M, Lee H L, Lee S W, Han N I, Kim S-H, Song M J, Hwang S, Sung P S, Jang J W, Bae S H, Choi J Y, Yoon S K
Department of Internal Medicine, Incheon St. Mary's Hospital, The Catholic University of Korea, Incehon, Korea.
Catholic University Liver Research Center, The Catholic University of Korea, Seoul, Korea.
J Viral Hepat. 2018 Oct;25(10):1189-1196. doi: 10.1111/jvh.12918. Epub 2018 May 17.
Patients with chronic hepatitis C who achieve a sustained viral response after pegylated interferon therapy have a reduced risk of hepatocellular carcinoma, but the risk after treatment with direct-acting antivirals is unclear. We compared the rates of early development of hepatocellular carcinoma after direct-acting antivirals and after pegylated interferon therapy. We retrospectively analysed 785 patients with chronic hepatitis C who had no history of hepatocellular carcinoma (211 treated with pegylated interferon, 574 with direct-acting antivirals) and were followed up for at least 24 weeks after antiviral treatment. De novo hepatocellular carcinoma developed in 6 of 574 patients receiving direct-acting antivirals and in 1 of 211 patients receiving pegylated interferon. The cumulative incidence of early hepatocellular carcinoma development did not differ between the treatment groups either for the whole cohort (1.05% vs 0.47%, P = .298) or for those patients with Child-Pugh Class A cirrhosis (3.73% vs 2.94%, P = .827). Multivariate analysis indicated that alpha-fetoprotein level >9.5 ng/mL at the time of end-of-treatment response was the only independent risk factor for early development of hepatocellular carcinoma in all patients (P < .0001, hazard ratio 176.174, 95% confidence interval 10.768-2882.473) and in patients treated with direct-acting agents (P < .0001, hazard ratio 128.402, 95% confidence interval 8.417-1958.680). In conclusion, the rate of early development of hepatocellular carcinoma did not differ between patients treated with pegylated interferon and those treated with direct-acting antivirals and was associated with the serum alpha-fetoprotein level at the time of end-of-treatment response.
接受聚乙二醇干扰素治疗后获得持续病毒学应答的慢性丙型肝炎患者发生肝细胞癌的风险降低,但直接抗病毒药物治疗后的风险尚不清楚。我们比较了直接抗病毒药物治疗和聚乙二醇干扰素治疗后肝细胞癌的早期发生几率。我们回顾性分析了785例无肝细胞癌病史的慢性丙型肝炎患者(211例接受聚乙二醇干扰素治疗,574例接受直接抗病毒药物治疗),并在抗病毒治疗后至少随访24周。接受直接抗病毒药物治疗的574例患者中有6例发生了新发肝细胞癌,接受聚乙二醇干扰素治疗的211例患者中有1例发生了新发肝细胞癌。整个队列中,治疗组间早期肝细胞癌发生的累积发生率无差异(1.05%对0.47%,P = 0.298);Child-Pugh A级肝硬化患者中,治疗组间早期肝细胞癌发生的累积发生率也无差异(3.73%对2.94%,P = 0.827)。多因素分析表明,治疗结束时应答时甲胎蛋白水平>9.5 ng/mL是所有患者(P < 0.0001,风险比176.174,95%置信区间10.768 - 2882.473)以及接受直接抗病毒药物治疗患者(P < 0.0001,风险比128.402,95%置信区间8.417 - 1958.680)早期发生肝细胞癌的唯一独立危险因素。总之,聚乙二醇干扰素治疗患者和直接抗病毒药物治疗患者的肝细胞癌早期发生率无差异,且与治疗结束时应答时的血清甲胎蛋白水平相关。