Cachexia in rheumatoid arthritis is not explained by decreased growth hormone secretion

Laura C. Rall, Joseph M. Walsmith, Laura Snydman, Seymour Reichlin, Johannes D. Veldhuis, Joseph J. Kehayias, Leslie W. Abad, Nancy T. Lundgren, Ronenn Roubenoff

Research output: Contribution to journalArticlepeer-review

32 Scopus citations


Objective. 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." Methods. 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. Results. 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. Conclusion. These findings suggest that GH kinetics are unaltered in RA patients compared with healthy subjects; thus, GH deficiency does not account for rheumatoid cachexia.

Original languageEnglish (US)
Pages (from-to)2574-2577
Number of pages4
JournalArthritis and rheumatism
Issue number10
StatePublished - Oct 1 2002

ASJC Scopus subject areas

  • Immunology and Allergy
  • Rheumatology
  • Immunology
  • Pharmacology (medical)


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