Arase Y, Suzuki F, Suzuki Y, Akuta N, Kobayashi M, Kawamura Y, Yatsuji H, Sezaki H, Hosaka T, Hirakawa M, Saito S, Ikeda K, Kumada H. Hepatitis C virus enhances incidence of idiopathic pulmonary fibrosis. World J Gastroenterol 2008; 14(38): 5880-5886 [PMID: 18855988 DOI: 10.3748/wjg.14.5880]
Corresponding Author of This Article
Yasuji Arase, MD, Department of Hepatology, Toranomon Hospital, 2-2-2, Toranomon, Minato-ku, Tokyo 105-8470, Japan. es9y-ars@asahi-net.or.jp
Article-Type of This Article
Rapid Communication
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Yasuji Arase, Fumitaka Suzuki, Yoshiyuki Suzuki, Norio Akuta, Masahiro Kobayashi, Yusuke Kawamura, Hiromi Yatsuji, Hitomi Sezaki, Tetsuya Hosaka, Miharu Hirakawa, Satoshi Saito, Kenji Ikeda, Hiromitsu Kumada, Department of Hepatology, Toranomon Hospital, Tokyo 105-8470, Japan
Author contributions: Arase Y contributed to design, data collection, data analysis, manuscript development and oversight; Suzuki F contributed to design, data collection, data analysis, manuscript development; Suzuki Y contributed to data collection; Akuta N contributed to data collection; Kobayashi M contributed to data collection; Kawamura Y contributed to data collection; Yatsuji H contributed to data collection; Sezaki H contributed to data collection; Hosaka T contributed to data collection; Hirakawa M contributed to data collection; Saito S contributed to data collection; Ikeda K contributed to data collection; Kumada H contributed to design, data collection, data analysis, manuscript development and oversight.
Supported by Grants-in-Aid from Okinaka Memorial Institute for Medical Research and the Japanese Ministry of Health, Labour and Welfare
Correspondence to: Yasuji Arase, MD, Department of Hepatology, Toranomon Hospital, 2-2-2, Toranomon, Minato-ku, Tokyo 105-8470, Japan. es9y-ars@asahi-net.or.jp
Telephone: +81-3-3588-1111 Fax: +81-3-3582-7068
Received: May 7, 2008 Revised: August 18, 2008 Accepted: August 25, 2008 Published online: October 14, 2008
Abstract
AIM: To investigate the cumulative development incidence and predictive factors for idiopathic pulmonary fibrosis in hepatitis C virus (HCV) positive patients.
METHODS: We studied 6150 HCV infected patients who were between 40-70 years old (HCV-group). Another 2050 patients with hepatitis B virus (HBV) were selected as control (HBV-group). The mean observation period was 8.0 ± 5.9 years in HCV-group and 6.3 ± 5.5 years in HBV-group. The primary goal is the development of idiopathic pulmonary fibrosis (IPF) in both groups. The cumulative appearance rate of IPF and independent factors associated with the incidence rate of IPF were calculated using the Kaplan-Meier method and the Cox proportional hazard model. All of the studies were performed retrospectively by collecting and analyzing data from the patient records in our hospital.
RESULTS: Fifteen patients in HCV-group developed IPF. On the other hand, none of the patients developed IPF in HBV-group. In HCV-group, the cumulative rates of IPF development were 0.3% at 10th year and 0.9% at 20th year. The IPF development rate in HCV-group was higher than that in HBV-group (P = 0.021). The IPF development rate in patients with HCV or HBV was high with statistical significance in the following cases: (1) patients ≥ 55 years (P < 0.001); (2) patients who had smoking index (package per day × year) of ≥ 20 (P = 0.002); (3) patients with liver cirrhosis (P = 0.042).
CONCLUSION: Our results indicate that age, smoking and liver cirrhosis enhance the development of IPF in HCV positive patients.