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Hepatic steatosis in chronic hepatitis C is a significant risk factor for developing hepatocellular carcinoma independent of age, sex, obesity, fibrosis stage and response to interferon therapy
Author(s) -
Kurosaki Masayuki,
Hosokawa Takanori,
Matsunaga Kotaro,
Hirayama Itsuko,
Tanaka Tomohiro,
Sato Mitsuaki,
Yasui Yutaka,
Tamaki Nobuharu,
Ueda Ken,
Tsuchiya Kaoru,
Kuzuya Teiji,
Nakanishi Hiroyuki,
Itakura June,
Takahashi Yuka,
Asahina Yasuhiro,
Enomoto Nobuyuki,
Izumi Namiki
Publication year - 2010
Publication title -
hepatology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.123
H-Index - 75
eISSN - 1872-034X
pISSN - 1386-6346
DOI - 10.1111/j.1872-034x.2010.00692.x
Subject(s) - steatosis , medicine , hepatocellular carcinoma , gastroenterology , body mass index , risk factor , steatohepatitis , hepatitis c , fibrosis , stage (stratigraphy) , fatty liver , disease , paleontology , biology
Aim: Hepatic steatosis is linked to development of hepatocellular carcinoma (HCC) in non‐viral liver disease such as non‐alcoholic steatohepatitis. The present study aimed to assess whether hepatic steatosis is associated with the development of HCC in chronic hepatitis C. Methods: We studied a retrospective cohort of 1279 patients with chronic hepatitis C who received interferon (IFN) therapy between 1994 and 2005 at a single regional hospital in Japan. Of these patients, 393 had a sustained virological response (SVR) and 886 had non‐SVR to IFN therapy. After IFN therapy, these patients were screened for development of HCC every 6 months. The average period of observation was 4.5 years. Results: HCC developed in 68 patients. The annual incidence of HCC was 2.73% for patients with a steatosis grade of 10% or greater and 0.69% for patients with a steatosis grade of 0–9%. On multivariate analysis, higher grade of steatosis was a significant risk factor for HCC independent of older age, male sex, higher body mass index (BMI), advanced fibrosis stage and non‐SVR to IFN therapy. The adjusted risk ratio of hepatic steatosis was 3.04 (confidence interval 1.82–5.06, P < 0.0001), which was higher than that of older age (1.09), male sex (2.12), non‐SVR to IFN (2.43) and higher BMI (1.69). Conclusion: Hepatic steatosis is a significant risk factor for development of HCC in chronic hepatitis C independent of other known risk factors, which suggest the possibility that amelioration of hepatic steatosis may prevent hepatocarcinogenesis.