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Volume 48, Issue 5, Pages 736-742 (May 2008)


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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

Masayuki Kurosaki1, Kotaro Matsunaga1, Itsuko Hirayama1, Tomohiro Tanaka1, Mitsuaki Sato1, Nobutoshi Komatsu1, Naoki Umeda1, Takanori Hosokawa1, Ken Ueda1, Kaoru Tsuchiya1, Hiroyuki Nakanishi1, Jun Itakura1, Yasuhiro Asahina1, Shozo Miyake1, Nobuyuki Enomoto2, Namiki Izumi1Corresponding Author Informationemail address

Received 20 July 2007; received in revised form 8 October 2007; accepted 17 December 2007. published online 26 February 2008.

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.

Associate Editor: J.G. McHutchison

KeywordsSteatosis, ALT, Fibrosis

1 Division of Gastroenterology and Hepatology, Musashino Red Cross Hospital, 1-26-1 Kyonan-cho, Musashino-shi, Tokyo 180-8610, Japan

2 First Department of Internal Medicine, University of Yamanashi, Yamanashi, Japan

Corresponding Author InformationCorresponding author. Tel.: +81 422 32 3111; fax: +81 422 32 9551.

 The authors who have taken part in the research of this paper declared that they do not have a relationship with the manufactures of the drug involved either in the past or present and they did not receive funding from the manufactures to carry out their research. They did not receive funding from any source to carry out this study.

PII: S0168-8278(08)00122-0

doi:10.1016/j.jhep.2007.12.025


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