Nancy T. Lundgren is deceased.
Cachexia in rheumatoid arthritis is not explained by decreased growth hormone secretion†
Version of Record online: 16 OCT 2002
Copyright © 2002 by the American College of Rheumatology
Arthritis & Rheumatism
Volume 46, Issue 10, pages 2574–2577, October 2002
How to Cite
Rall, L. C., Walsmith, J. M., Snydman, L., Reichlin, S., Veldhuis, J. D., Kehayias, J. J., Abad, L. W., Lundgren, N. T. and Roubenoff, R. (2002), Cachexia in rheumatoid arthritis is not explained by decreased growth hormone secretion. Arthritis & Rheumatism, 46: 2574–2577. doi: 10.1002/art.10714
The contents of this publication do not necessarily reflect the views or policies of the US Department of Agriculture, nor does mention of trade names, commercial products, or organizations imply endorsement by the US government.
- Issue online: 16 OCT 2002
- Version of Record online: 16 OCT 2002
- Manuscript Accepted: 27 JUN 2002
- Manuscript Received: 30 NOV 2001
- NIH. Grant Numbers: DK-02120, RR-00054
- Arthritis Foundation Clinical Science
- USDA cooperative agreement. Grant Number: 58-1950-9-001
Patients with rheumatoid arthritis (RA) lose body cell mass (BCM) by unknown mechanisms. Since the loss of BCM in normal aging individuals parallels the characteristic age-related decline in growth hormone (GH) secretion, this study was carried out to determine whether further decreased GH secretion plays a role in the pathogenesis of this loss of BCM in RA patients, termed “rheumatoid cachexia.”
GH secretory kinetics were determined by deconvolution analysis in 16 patients with RA and 17 healthy controls matched for age (mean ± SD 45.4 ± 13.2 years and 47.1 ± 14.6 years, respectively), sex, race, and body mass index. Blood samples were obtained every 20 minutes for 24 hours. Body composition was ascertained using total-body potassium (TBK) as a measure of BCM and dual x-ray absorptiometry to determine fat mass.
BCM was reduced in patients with RA compared with healthy controls (mean ± SD gm TBK 79.5 ± 9.5 versus 94.9 ± 11.9; P < 0.0005), but there was no difference in fat mass. GH kinetic parameters in patients with RA did not differ from those in controls.
These findings suggest that GH kinetics are unaltered in RA patients compared with healthy subjects; thus, GH deficiency does not account for rheumatoid cachexia.