OBJECTIVE: To evaluate the effects of glucocorticoids on cardiovascular (CV) risk in rheumatoid arthritis (RA). 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.
OBJECTIVE: To evaluate the effects of glucocorticoids on cardiovascular (CV) risk in rheumatoid arthritis (RA). METHODS: We recorded demographic, clinical, disease outcome, and treatment variables in 92 consecutive RApatients 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.
Authors: Cynthia S Crowson; Katherine P Liao; John M Davis; Daniel H Solomon; Eric L Matteson; Keith L Knutson; Mark A Hlatky; Sherine E Gabriel Journal: Am Heart J Date: 2013-08-29 Impact factor: 4.749
Authors: Tracey E Toms; Vasileios F Panoulas; Karen M J Douglas; Helen R Griffiths; George D Kitas Journal: Arthritis Res Ther Date: 2008-12-17 Impact factor: 5.156