Search J Rheum

Advanced Search

Home

Current Issue

Archives

Guidelines for Authors

Classified Ads

Links

Search PubMed

Subscriptions

Subscriber Registration

Guidelines for Website Users

JRheum Update Service

Contact Info


Read Full Text


Download PDF


View Table of Contents

Role of Endothelial Damage in the Pathogenesis of Interstitial Pneumonitis in Patients with Polymyositis and Dermatomyositis

MASANORI FUNAUCHI, HIDEKI SHIMADSU, CHISE TAMAKI, TOSHIAKI YAMAGATA, YUJI NOZAKI, MASAFUMI SUGIYAMA, SHINYA IKOMA, and KOJI KINOSHITA

ABSTRACT.

Objective. Polymyositis and dermatomyositis (PM/DM) are often complicated by interstitial pneumonitis (IP), which is an important cause of death. It has been reported that blood concentration of transforming growth factor-ß (TGF-ß), which is produced by a wide range of cells including endothelial cells and enhances the fibrotic changes in various tissues, is increased in PM/DM with IP. Endothelial damage is likely to exist in PM/DM. We studied the relationship between endothelial damage and IP in PM/DM.

Methods. Blood levels of sialylated carbohydrate antigen KL-6, TGF-ß, endothelin-1 (ET-1), thrombomodulin (TM), and plasminogen activator inhibitor-1 (PAI-1) were determined in 43 patients with PM or DM with or without IP, and the relationship between these measures was analyzed.

Results. Blood levels of KL-6 and TGF-ß were higher in the patients with IP than those without, and these measures were well correlated with each other. Levels of ET-1, TM, and PAI-1, all known to reflect the extent of endothelial damage, were also increased in patients with IP, and these measures correlated well with TGF-ß.

Conclusion. Our data suggest that endothelial damage might play an important role through the production of fibrosis-enhancing factors such as TGF-ß or ET-1 in PM/DM. (J Rheumatol 2006;33:903–6)

Key Indexing Terms:

INTERSTITIAL PNEUMONITIS
TRANSFORMING GROWTH FACTOR-ß
ENDOTHELIAL DAMAGE
POLYMYOSITIS
DERMATOMYOSITIS


From the Department of Nephrology and Rheumatology, Kinki University School of Medicine, Osaka, Japan.

M. Funauchi, MD; H. Shimadsu; C. Tamaki; T. Yamagata, MD; Y. Nozaki, MD; M. Sugiyama, MD; S. Ikoma, MD; K. Kinoshita, MD.

Address reprint requests to Dr. M. Funauchi, Department of Nephrology and Rheumatology, Kinki University School of Medicine, 377-2 Ohno-Higashi, Osaka-Sayama 589-8511, Osaka, Japan. E-mail: funauchi@med.kindai.ac.jp

Accepted for publication December 16, 2005.




Return to May 2006 Table of Contents



© 2006. The Journal of Rheumatology Publishing Company Limited.
All rights reserved.