Moriyama Mitsuhiko, Matsumura Hiroshi, Aoki Hiroshi, Shimizu Toshihiro, Yamagami Hiroaki, Shioda Atsuo, Kaneko Miki, Goto Iori, Tanaka Naohide, Arakawa Yasuyuki
Division of Gastroenterology and Hepatology, Department of Medicine, Nihon University School of Medicine, Itabashi-ku, Tokyo 173-8610, Japan.
Liver Int. 2005 Feb;25(1):85-90. doi: 10.1111/j.1478-3231.2005.01028.x.
The incidence of hepatocellular carcinoma (HCC) in C-viral chronic hepatitis (CH) and liver cirrhosis (LC) patients after interferon (IFN) therapy was evaluated according to alanine aminotransferase (ALT) levels.
Two hundred sixty-nine patients with C-viral CH and LC were treated with natural IFN-alpha. The efficacy of IFN therapy was evaluated based on virologic response and ALT levels using the following groups: virologic-sustained responders (VSR); biochemical-sustained responders (BSR); partial responders (PR), which consisted of BSR patients whose serum ALT levels later relapsed; non-responders (NR)1, which included patients with serum ALT levels that were usually less than 80 IU/l; and NR2, NR with ALT levels persistently more than 80 IU/l.
Of the 269 patients, 22 (8.2%) developed HCC after IFN therapy. The incidence of HCC (%/patient/year) was 0.78%, 0%, 0%, 0.17%, 4.68% in VSR, BR, PR, NR1, NR2, respectively. Multivariate analysis revealed that an increase in ALT levels to more than 80 IU/l is an important risk factor for the occurrence of HCC.
We concluded that the patients with ALT levels less than twice the upper limit of normal after IFN therapy have a reduced risk of progression to HCC from C-viral chronic liver disease.
根据丙氨酸氨基转移酶(ALT)水平,评估丙型病毒性慢性肝炎(CH)和肝硬化(LC)患者接受干扰素(IFN)治疗后肝细胞癌(HCC)的发生率。
269例丙型病毒性CH和LC患者接受了天然α干扰素治疗。根据病毒学反应和ALT水平,将IFN治疗的疗效分为以下几组进行评估:病毒学持续应答者(VSR);生化持续应答者(BSR);部分应答者(PR),包括血清ALT水平随后复发的BSR患者;无应答者(NR)1,包括血清ALT水平通常低于80 IU/L的患者;以及NR2,ALT水平持续高于80 IU/L的无应答者。
269例患者中,22例(8.2%)在IFN治疗后发生HCC。HCC的发生率(%/患者/年)在VSR、BR、PR、NR1、NR2组中分别为0.78%、0%、0%、0.17%、4.68%。多因素分析显示,ALT水平升高至超过80 IU/L是发生HCC的重要危险因素。
我们得出结论,IFN治疗后ALT水平低于正常上限两倍的患者,从丙型病毒性慢性肝病进展为HCC的风险降低。