title: The effect of disease activity on body composition and resting energy expenditure in patients with rheumatoid arthritis.
abstract: BACKGROUND
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: University of Manchester, Rheumatic Diseases Centre, Salford Royal Hospitals NHS Trust, Salford, UK.
authors.forename: K
authors.initials: K
authors.lastname: Binymin
authors.forename: Al
authors.initials: A
authors.lastname: Herrick
authors.forename: Gl
authors.initials: G
authors.lastname: Carlson
authors.forename: Sj
authors.initials: S
authors.lastname: Hopkins
references.citation: Arch Intern Med. 2005 Jul 25;165(14):1624-9
references.pmid: 16043681
references.citation: Rheumatology (Oxford). 2009 Sep;48(9):1128-32
references.pmid: 19602478
references.citation: Curr Pharm Des. 2007;13(35):3637-47
references.pmid: 18220800
references.citation: N Engl J Med. 1994 Mar 3;330(9):602-5
references.pmid: 8302342
references.citation: Nutrition. 1990 May-Jun;6(3):213-21
references.pmid: 2136000
references.citation: Clin Rheumatol. 2009 Apr;28(4):439-44
references.pmid: 19096748
references.citation: Rheumatology (Oxford). 2007 Dec;46(12):1824-7
references.pmid: 18032540
references.citation: Rheumatology (Oxford). 2008 Aug;47(8):1124-31
references.pmid: 18448480
references.citation: Cancer Res. 1992 Aug 1;52(15):4113-6
references.pmid: 1638523
references.citation: Br J Nutr. 1974 Jul;32(1):77-97
references.pmid: 4843734
references.citation: Arthritis Rheum. 1995 Jan;38(1):44-8
references.pmid: 7818570
references.citation: Am J Clin Nutr. 2006 Apr;83(4):735-43
references.pmid: 16600922
references.citation: J Nutr. 1995 Sep;125(9):2333-40
references.pmid: 7666250
references.citation: Arthritis Rheum. 2008 Jun 15;59(6):807-15
references.pmid: 18512711
references.citation: Scand J Rheumatol. 2008 Sep-Oct;37(5):321-8
references.pmid: 18666027
references.citation: Eur J Nutr. 2009 Aug;48(5):315-22
references.pmid: 19333642
references.citation: J Rheumatol. 1982 Sep-Oct;9(5):789-93
references.pmid: 7175852
references.citation: Eur J Clin Invest. 1991 Oct;21(5):479-84
references.pmid: 1752286
references.citation: Clin Nutr. 2010 Apr;29(2):154-9
references.pmid: 20060626
references.citation: Arthritis Rheum. 1983 Nov;26(11):1346-53
references.pmid: 6639693
references.citation: Arthritis Rheum. 1988 Jun;31(6):784-8
references.pmid: 3260102
references.citation: Oncol Rep. 2005 Jul;14(1):257-63
references.pmid: 15944798
references.citation: Blood. 1994 Oct 15;84(8):2472-9
references.pmid: 7919367
references.citation: Arthritis Rheum. 1988 Mar;31(3):315-24
references.pmid: 3358796
references.citation: Eur J Clin Invest. 1987 Dec;17(6):504-10
references.pmid: 3123250
references.citation: Curr Opin Clin Nutr Metab Care. 2003 Jan;6(1):15-20
references.pmid: 12496676
references.citation: Scand J Rheumatol. 1988;17(6):469-74
references.pmid: 3266031
references.citation: Arthritis Rheum. 1989 May;32(5):531-7
references.pmid: 2719728
references.citation: Nutr Cancer. 2001;40(2):118-24
references.pmid: 11962246
references.citation: N Engl J Med. 1983 Mar 10;308(10):545-52
references.pmid: 6828080