The objective of this study is to determine the causes and predictors of death in systemic lupus erythematosus (SLE) patients. Causes of death were defined based on death certificates, medical records, and information collected from doctors and relatives. Possible variables predicting mortality were assessed by Kaplan-Meier and Cox regression methods. The multivariate model was validated using the bootstrap method, and the hazard ratios were adjusted according to the shrinkage coefficient. One hundred eighty-one patients were included, and two patients were lost to follow-up. The median (IR) age at T (0) and disease duration of the 179 patients were 26.7 (21.8-34.6) and 8.2 (4.3-12.4) years, respectively. After a median (IR) follow-up of 3.3 (3.1-3.5) years, 13 (7.3 %) patients died due to end-organ failure (5), infection (5), disease activity (1), and atherosclerotic cardiovascular disease (CVD) (1). The cause of mesenteric ischemia in one patient could not be determined. Predictors of mortality collected at T(0) were the following: nephritis, chronic kidney disease, antiphospholipid syndrome (APS), higher modified SLEDAI-2k, higher damage index score, intravenous cyclophosphamide use, higher daily dose of prednisone, and higher systolic blood pressure. Independent predictors of mortality were higher damage index score (HR: 1.40; 95 % CI: 1.08-1.82), cyclophosphamide use (HR: 3.80; 95 % CI: 1.13-12.77), and APS diagnosis (HR: 3.82; 95 % CI: 1.07-13.59). This paper presents a high frequency of late mortality in lupus patients due to the SLE itself and infection. This result is not in agreement with the initial proposed bimodal pattern of lupus mortality, nor is it in agreement with the high frequency of CVD as a cause of death in developed countries. The most important predictors of death were related to the lupus itself.
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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