The effect of disease activity on body composition and resting energy expenditure in patients with rheumatoid arthritis

Introduction: Cachexia is associated with rheumatoid arthritis (RA), but whether it is attributable primarily to reduced dietary intake or increased metabolism is unclear, as is the association with inflammation. To examine whether rheumatoid cachexia is related to increased energy expenditure, reduced food intake, or an inflammatory cytokine response we undertook a prospective, longitudinal study of patients with RA, during periods of relative relapse and remission of inflammation. Methods: Sixteen patients admitted to hospital with a flare of RA were assessed clinically to determine disease activity and were re-examined 6 weeks later. Their fat-free mass (FFM), dietary intake, resting energy expenditure (REE), and plasma concentrations of interleukin-6 (IL-6) were also measured. Data were compared with those from 16 healthy, age- and sex-matched controls. Results: At baseline the body weight, body mass index, and FFM of patients with RA were significantly lower than those of controls. Disease activity scores of patients (6.39 +/- 0.8) were reduced when the patients were re-examined 6 weeks later (5.23 +/- 1.26) and FFM was no longer statistically different from that of controls (visit 1 = 25.8 +/- 10.1 and visit 2 = 26.8 +/- 9.5 versus controls = 32.3 +/- 10.9). There were no differences in food intake between patients and controls or between patients studied at the 2 time points, but REE was greater in patients after correcting for FMM (visit 1 = 62.2 +/- 24.7, visit 2 = 59.7 +/- 26.3 versus controls = 46.0 +/- 13.7). Plasma IL-6 concentrations were significantly higher in patients than controls. Although IL-6 was not significantly correlated with REE, lower REE measurements were not observed when the plasma IL-6 concentration increased. Conclusion: Reduced FFM in patients with RA is not attributable to reduced food intake. Energy expenditure is greater in patients when corrected for FFM, particularly in patients with acute flares of disease activity. Although clearly not the only factor involved, increased production of IL-6 may contribute to increasing REE.