PT  - JOURNAL ARTICLE
AU  - Dessein, Patrick H
AU  - Norton, Gavin R
AU  - Woodiwiss, Angela J
AU  - Joffe, Barry I
AU  - Solomon, Ahmed
TI  - Independent role of conventional cardiovascular risk factors as predictors of C-reactive protein concentrations in rheumatoid arthritis.
DP  - 2007 Apr 01
TA  - The Journal of Rheumatology
PG  - 681--688
VI  - 34
IP  - 4
4099  - http://www.jrheum.org/content/34/4/681.short
4100  - http://www.jrheum.org/content/34/4/681.full
SO  - J Rheumatol2007 Apr 01; 34
AB  - OBJECTIVE: We elucidated whether factors that determine systemic inflammation in the general population independently contribute to C-reactive protein (CRP) concentrations in rheumatoid arthritis (RA). METHODS: The association between factors known to be associated with systemic inflammation in the general population (age, sex, lifestyle variables, metabolic syndrome features, and estrogen use) and high sensitivity CRP (hs-CRP) concentrations independent of the Disease Activity Score 28 (DAS28) was determined in 94 patients with RA. RESULTS: In all patients, the DAS28 (p < 0.0001), ever smoking (p <or= 0.006), waist circumference (p = 0.03), and the homeostasis model assessment of insulin resistance (HOMA-IR; p = 0.03) were independently associated with hs-CRP. Although in patients without central obesity (n = 53, 56%), the DAS28 was the only independent predictor of inflammation and contributed 28%-30% to the variability of hs-CRP, in patients with National Cholesterol Education Program (NCEP) defined central obesity (n = 41, 44%), smoking contributed 13%, the HOMA-IR 21%, and the DAS28 21% to the variability of hs-CRP. In centrally obese patients, the standardized regression coefficient for the independent relationship between HOMA-IR and hs-CRP (0.401 +/- 0.132) was similar to that for DAS28 and hs-CRP (0.432 +/- 0.144); and the HOMA-IR (p = 0.04) was associated with hs-CRP independent of waist circumference. CONCLUSION: In patients with RA with NCEP-defined central obesity, insulin resistance explains a degree of the variability of CRP concentrations equivalent to that of disease activity. These findings have potential implications for the use of CRP as an RA disease activity marker, and in understanding the reported relationship of CRP with cardiovascular disease in RA.