The presence of steatosis and elevation of alanine aminotransferase levels are associated with fibrosis progression in chronic hepatitis C with non-response to interferon therapy

被引:32
作者
Kurosaki, Masayuki [1 ]
Matsunaga, Kotaro [1 ]
Hirayama, Itsuko [1 ]
Tanaka, Tomohiro [1 ]
Sato, Mitsuaki [1 ]
Komatsu, Nobutoshi [1 ]
Umeda, Naoki [1 ]
Hosokawa, Takanori [1 ]
Ueda, Ken [1 ]
Tsuchiya, Kaoru [1 ]
Nakanishi, Hiroyuki [1 ]
Itakura, Jun [1 ]
Asahina, Yasuhiro [1 ]
Miyake, Shozo [1 ]
Enomoto, Nobuyuki [2 ]
Izumi, Namiki [1 ]
机构
[1] Musashino Red Cross Hosp, Div Gastroenterol & Hepatol, Musashino, Tokyo 1808610, Japan
[2] Univ Yamanashi, Dept Internal Med 1, Yamanashi, Japan
关键词
steatosis; ALT; fibrosis;
D O I
10.1016/j.jhep.2007.12.025
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background/Aims: Interferon (IFN) therapy leads to regression of hepatic fibrosis in chronic hepatitis C patients who achieve a sustained virologic response (SVR), while the beneficial effect is limited in those who fail to do so. The aim of the present study was to define factors associated with progression of fibrosis in patients who do not achieve a SVR. Methods: Fibrosis staging scores were compared between paired liver biopsies before and after IFN in 97 chronic hepatitis C patients who failed therapy. The mean interval between biopsies was 5.9 years. Factors associated with progression of fibrosis were analyzed. Results: Fibrosis progressed in 23%, remained unchanged in 47% and regressed in 29%. Steatosis and a high average alanine aminotransferase (ALT) between biopsies were independent factors for progression of fibrosis with risk ratios of 5.53 and 4.48, respectively. Incidence and yearly rate of progression of fibrosis was 64% and 0.22 +/- 0.29 fibrosis units per year in those with both risk factors compared to 8% and -0.04 +/- 0.17 fibrosis units per year in those negative for both factors. Conclusions: Hepatic steatosis and elevated ALT levels are risk factors for progression of fibrosis in chronic hepatitis C patients who fail to achieve a SVR to IFN therapy and therefore may be therapeutic targets to halt the potentially progressive disease. (C) 2008 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:736 / 742
页数:7
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