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Independent Role of Conventional Cardiovascular Risk Factors as Predictors of C-Reactive Protein Concentrations in Rheumatoid Arthritis
PATRICK H. DESSEIN, GAVIN R. NORTON, ANGELA J. WOODIWISS, BARRY I. JOFFE, and AHMED SOLOMON ABSTRACT. 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 ≤ 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. (First Release Jan 31 2007; J Rheumatol 2007;34:681–8) Key Indexing Terms:
RHEUMATOID ARTHRITIS From the Department of Rheumatology, Johannesburg Hospital and Milpark Hospital, Parktown, University of the Witwatersrand; Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand; and the Centre for Diabetes and Endocrinology, Houghton, University of the Witwatersrand, Johannesburg, South Africa. P.H. Dessein, MD, FCP(SA), PhD; A. Solomon, FCP(SA), Department of Rheumatology, Johannesburg Hospital and Milpark Hospital; G.R. Norton, MBBCh, PhD; A.J. Woodiwiss, PhD, Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences; B.I. Joffe, DSc, Centre for Diabetes and Endocrinology, University of the Witwatersrand. Address reprint requests to Dr. P.H. Dessein, PO Box 1012, Melville 2109, Johannesburg, South Africa. E-mail: Dessein@telkomsa.net Accepted for publication December 11, 2006.
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