Liver Cancer
Copyright ©2007 Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Oct 21, 2007; 13(39): 5180-5187
Published online Oct 21, 2007. doi: 10.3748/wjg.v13.i39.5180
Hepatic steatosis as a possible risk factor for the development of hepatocellular carcinoma after eradication of hepatitis C virus with antiviral therapy in patients with chronic hepatitis C
Atsushi Tanaka, Satoko Uegaki, Hiroko Kurihara, Kiyoshi Aida, Masaki Mikami, Ikuo Nagashima, Junji Shiga, Hajime Takikawa
Atsushi Tanaka, Satoko Uegaki, Hiroko Kurihara, Masaki Mikami, Hajime Takikawa, Department of Medicine, Teikyo University School of Medicine, Kaga, Itabashi-ku, Tokyo 173-8605, Japan
Kiyoshi Aida, Junji Shiga, Department of Pathology, Teikyo University School of Medicine, Kaga, Itabashi-ku, Tokyo 173-8605, Japan
Ikuo Nagashima, Department of Surgery, Teikyo University School of Medicine, Kaga, Itabashi-ku, Tokyo 173-8605, Japan
Author contributions: All authors contributed equally to the work.
Correspondence to: Atsushi Tanaka, MD, Department of Medicine, Teikyo University School of Medicine, 2-11-1, Kaga, Itabashi-ku, Tokyo 173-8605, Japan. a-tanaka@med.teikyo-u.ac.jp
Telephone: +81-3-39641211 Fax: +81-3-53751308
Received: April 18, 2007
Revised: June 28, 2007
Accepted: September 1, 2007
Published online: October 21, 2007
Abstract

AIM: To elucidate risk factors contributing to the development of hepatocellular carcinoma (HCC) among patients with sustained viral response (SVR) after interferon (IFN) treatment and to examine whether HCV-RNA still remained in the liver of SVR patients who developed HCC.

METHODS: Two-hundred and sixty-six patients, who achieved SVR, were enrolled in this study. We retrospectively reviewed clinical, viral and histological features of the patients, and examined whether the development of HCC depends on several clinical variables using Kaplan-Meier Method. RT-PCR was used to seek HCV-RNA in 3 out of 7 patients in whom liver tissue was available for molecular analysis.

RESULTS: Among the enrolled 266 patients with SVR, HCC developed in 7 patients (7/266; 2.6%). We failed to detect HCV-RNA both in cancer and non-cancerous liver tissue in all three patients. The cumulative incidence for HCC was significantly different depending on hepatic fibrosis (F3-4) (P = 0.0028), hepatic steatosis (Grade 2-3) (P = 0.0002) and age (≥ 55) (P = 0.021) at the pre-interferon treatment.

CONCLUSION: The current study demonstrated that age, hepatic fibrosis, and hepatic steatosis at pre-interferon treatment might be risk factors for developing HCC after SVR.

Keywords: Hepatitis C virus, Chronic hepatitis C, Hepatocellular carcinoma, Hepatic steatosis, Hepatic fibrosis, Interferon therapy, Sustained viral response