Clinical Research
Copyright ©The Author(s) 2004. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Mar 15, 2004; 10(6): 894-898
Published online Mar 15, 2004. doi: 10.3748/wjg.v10.i6.894
Fenofibrate for patients with asymptomatic primary biliary cirrhosis
Kazufumi Dohmen, Toshihiko Mizuta, Makoto Nakamuta, Naoya Shimohashi, Hiromi Ishibashi, Kyosuke Yamamoto
Kazufumi Dohmen, Department of Internal Medicine, Okabe Hospital, Japan
Hiromi Ishibashi, Department of Clinical Research Center, National Nagasaki Medical Center, Japan
Toshihiko Mizuta, Kyosuke Yamamoto, Department of Internal Medicine, Saga Medical School, Japan
Makoto Nakamuta, Department of Medicine and Bioregultory Science, Graduate School of Medical Sciences, Kyushu University, Japan
Naoya Shimohashi, Department of Internal Medicine, Fukuoka City Hospital, Japan
Author contributions: All authors contributed equally to the work.
Correspondence to: Dr. Kazufumi Dohmen, Department of Internal Medicine, Okabe Hospital, 1-2-1 Myojinzaka Umi-machi Kasuya-gun Fukuoka 811-2122 Japan. dohmenk@par.odn.ne.jp
Telephone: +81-92-932-0025 Fax: +81-92-933-7253
Received: November 17, 2003
Revised: November 23, 2003
Accepted: January 18, 2004
Published online: March 15, 2004
Abstract

AIM: Primary biliary cirrhosis (PBC) is a chronic, cholestatic disease of autoimmune etiology, the histology of which shows a destruction of the intrahepatic bile duct and portal inflammation. Ursodeoxycholic acid (UDCA) is now used as a first-line drug for asymptomatic PBC (aPBC) because it is reported that UDCA decreases mortality and prolongs the time of liver transplantation. However, only 20-30% of patients respond fully to UDCA. Recently, lipoprotein-lowering agents have been found to be effective for PBC. The aim of this study was to examine the safety and efficacy of fenofibrate, a member of the fibrate class of hypolipidemic and anti-inflammatory agent via peroxysome proliferatory-activated receptor α, in patients with aPBC.

METHODS: Fenofibrate was administered for twelve weeks in nine patients with aPBC who failed to respond to UDCA. UDCA was used along with fenofibrate during the study. The data from aPBC patients were analyzed to assess the biochemical effect of fenofibrate during the study.

RESULTS: The serum levels of alkaline phosphatase (ALP) (285 ± 114.8 IU/L) and immunoglobulin M (IgM) (255.8 ± 85.9 mg/dl) significantly decreased to 186.9 ± 76.2 IU/L and 192.9 ± 67.5 mg/dL respectively, after fenofibrate treatment in patients with aPBC (P < 0.05). Moreover, the titer of antimitochondrial antibody (AMA) also decreased in 4 of 9 patients with aPBC. No adverse reactions were observed in any patients.

CONCLUSION: Fenofibrate appears to be significantly effective in treating patients with aPBC who respond incompletely to UDCA alone. Although the mechanism of fenofibrate on aPBC has not yet been fully clarified, combination therapy using fenofibrate and UDCA might be related to the anti-immunological effects, such as the suppression of AMA production as well as its anti-inflammatory effect.

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