Dr. Ascherman's work was supported by the NIH (grant K08-AR-047891); he also is a recipient of a National Arthritis Foundation Investigator award.
Anti–Jo-1 antibody levels correlate with disease activity in idiopathic inflammatory myopathy
Article first published online: 30 AUG 2007
Copyright © 2007 by the American College of Rheumatology
Arthritis & Rheumatism
Volume 56, Issue 9, pages 3125–3131, September 2007
How to Cite
Stone, K. B., Oddis, C. V., Fertig, N., Katsumata, Y., Lucas, M., Vogt, M., Domsic, R. and Ascherman, D. P. (2007), Anti–Jo-1 antibody levels correlate with disease activity in idiopathic inflammatory myopathy. Arthritis & Rheumatism, 56: 3125–3131. doi: 10.1002/art.22865
- Issue published online: 30 AUG 2007
- Article first published online: 30 AUG 2007
- Manuscript Accepted: 1 JUN 2007
- Manuscript Received: 9 NOV 2006
- NIH. Grant Number: K08-AR-047891
Previous case series have examined the relationship between anti–Jo-1 antibody levels and myositis disease activity, demonstrating equivocal results. Using enzyme-linked immunosorbent assays (ELISAs) and novel measures of myositis disease activity, the current study was undertaken to systematically reexamine the association between anti–Jo-1 antibody levels and various disease manifestations of myositis.
Serum anti–Jo-1 antibody levels were quantified using 2 independent ELISA methods, while disease activity was retrospectively graded using the Myositis Disease Activity Assessment Tool, which measures disease activity in 7 different organ systems via the Myositis Disease Activity Assessment Visual Analog Scale (VAS) and the Myositis Intention-to-Treat Index (MITAX) components. Spearman's rank correlation coefficients and mixed linear regression analysis were used to identify associations between anti–Jo-1 antibody levels and organ-specific disease activity in cross-sectional and longitudinal analyses, respectively.
Cross-sectional assessment of 81 patients with anti–Jo-1 antibody revealed a modest correlation between the anti–Jo-1 antibody level and the serum creatine kinase (CK) level, as well as muscle and joint disease activity. Correlation coefficients were similar for CK levels (rs = 0.38, P = 0.002), myositis VAS (rs = 0.36, P = 0.002), and arthritis VAS (rs = 0.40, P = 0.001). In multiple regression analyses of 11 patients with serial samples, anti–Jo-1 antibody levels correlated significantly with CK levels (R2 = 0.65, P = 0.0002), myositis VAS (R2 = 0.53, P = 0.0008), arthritis VAS (R2 = 0.53, P = 0.006), pulmonary VAS (R2 = 0.69, P = 0.005), global VAS (R2 = 0.63, P = 0.002), and global MITAX (R2 = 0.64, P = 0.0003).
In this large series of patients with idiopathic inflammatory myopathy, anti–Jo-1 antibody levels correlated modestly with muscle and joint disease, an association confirmed by a custom ELISA using recombinant human Jo-1. More striking associations emerged in a smaller longitudinal subset of patients that link anti–Jo-1 antibody levels to muscle, joint, lung, and global disease activity.