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Glucocorticoids and Insulin Sensitivity in
Rheumatoid Arthritis
PATRICK H. DESSEIN, BARRY I. JOFFE, ANNE E. STANWIX, BERENICE F. CHRISTIAN, and MARTIN VELLER
ABSTRACT. Methods. We recorded demographic, clinical, disease outcome, and treatment variables in 92 consecutive RA patients who were not taking lipid-lowering or antidiabetic medications. Fasting blood tests were taken for determination of lipids, ultra sensitive C-reactive protein (CRP), rheumatoid factor, insulin, and glucose. Insulin sensitivity was determined using the Quantitative Insulin Sensitivity Check Index (QUICKI). Results. Seventy-four (80%) patients were women, 80 Caucasian, 9 Asian, 2 of mixed ancestry and 1 Black. Their mean (95% confidence interval, CI) age, disease duration, and followup duration at our clinic were 56 (54-58), 11 (9-13) and 6 (5-6) years, respectively. Thirty-seven (40%) patients had received oral prednisone [cumulative dose 4.8 (2.0-8.5) g; duration one month to 20 years], and all patients had received pulsed (intraarticular, intramuscular, and/or intravenous) methylprednisolone [cumulative dose 2.0 (1.6-2.6) g]. Glucocorticoids were not associated with obesity, hypertension, or dyslipidemia. Having taken prednisone and high yearly frequencies of pulsed glucocorticoid administrations were associated with decreased insulin sensitivity (p < 0.05). After controlling for body mass index, ever having taken prednisone and high doses of pulsed glucocorticoids were independently associated with decreased insulin sensitivity (p < 0.05). Conclusion. Previous exposure to oral prednisone and high doses of pulsed glucocorticoids were associated with decreased insulin sensitivity in RA. Since decreased insulin sensitivity is an independent risk factor for CV disease, glucocorticoids may contribute to the excess CV event rates in RA. (J Rheumatol 2004;31:867-74) Key Indexing Terms:
RHEUMATOID ARTHRITIS
From the Departments of Rheumatology and Surgery, Johannesburg Hospital and Milpark Hospital, and the Centre for Diabetes and Endocrinology, the University of the Witwatersrand, Johannesburg, South Africa. P.H. Dessein, MD, FCP(SA); A.E. Stanwix, MRCP(UK); B.F. Christian, FCP(SA), Department of Rheumatology; M. Veller, FCS(SA), Department of Surgery, Johannesburg Hospital and Milpark Hospital; B.I. Joffe, DSc, Centre for Diabetes and Endocrinology University of the Witwatersrand. Address reprint requests to Dr. P.H. Dessein, P.O. Box 1012, Melville 2109, Johannesburg, South Africa. E-mail: Dessein@lancet.co.za Submitted June 11, 2003; revision accepted November 13, 2003. |