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Progression of carotid atherosclerosis in patients with systemic lupus erythematosus

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Abstract

The progression of carotid atherosclerosis in lupus patients is frequently encountered, and it is determined by both traditional and nontraditional risk factors. Of the 181 patients initially included in the study, 157 patients were reevaluated after 39(37–42) months. The progression of atherosclerosis was defined as the increase in the intima-media thickness (IMT) >0.15 mm and/or an increase of the plaque score. The predictive factors of progression were identified using the Poisson regression model. The median of the cohort age at baseline was 38 years (range 29–46 years; 96.2% female, 75.8% nonwhite). Carotid atherosclerosis progression was observed in 43 patients (27.4%), an increased plaque score was observed in nine patients (5.7%), an increase of IMT >0.15 mm was observed in 31 (19.7%), and both issues were present in three patients (1.9%). The univariate determinants of atherosclerosis progression were age, systemic lupus erythematosus (SLE) duration, and higher serum level of triglycerides (p < 0.05). The presence of nephrotic proteinuria (p = 0.063), stage 3 or greater chronic kidney disease (p = 0.091), and longer duration of prednisone use (p = 0.056) showed a tendency towards association with progression of atherosclerosis. The independent risk factors for progression were the SLE duration (p = 0.008, RR = 1.06, 95% CI = 1.03–1.10) and the presence of nephrotic proteinuria (p = 0.022, RR = 4.22, 95% CI = 2.18–8.15). The progression of atherosclerosis occurred in a substantial number of young SLE patients during a short-term follow-up. The independent factors associated with this progression emphasize the importance of SLE in determining atherosclerosis in these individuals.

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Pro-reitoria de Pesquisa da Universidade Federal de Minas Gerais.

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Correspondence to Antonio L. Ribeiro.

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Telles, R.W., Lanna, C.C.D., Sousa, A.J. et al. Progression of carotid atherosclerosis in patients with systemic lupus erythematosus. Clin Rheumatol 32, 1293–1300 (2013). https://doi.org/10.1007/s10067-013-2264-9

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  • DOI: https://doi.org/10.1007/s10067-013-2264-9

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