C David1, G Divard1, R Abbas2, B Escoubet3, J Chezel1, M P Chauveheid1, D Rouzaud1, A Boutten4, T Papo1,5,6, M Dehoux4, K Sacre1,5,6. 1. Departement of Internal Medicine, Bichat Hospital, University of Paris Diderot, PRES Sorbonne Paris Cité, APHP, Public Hospitals of Paris, Paris, France. 2. Department of Epidemiology and Clinical Research, Bichat Hospital, University of Paris Diderot, PRES Sorbonne Paris Cité, APHP, Public Hospitals of Paris, Paris, France. 3. Departement of Physiology, Bichat Hospital, University of Paris Diderot, PRES Sorbonne Paris Cité, APHP, Public Hospitals of Paris, INSERM, Paris, France. 4. Department of Metabolic and Cellular Biochemistry, Bichat Hospital, University of Paris Diderot, PRES Sorbonne Paris Cité, APHP, Public Hospitals of Paris, Paris, France. 5. INSERM U1149 (French Institute of Health and Medical Research), University of Paris Diderot, Paris, France. 6. Hospital-University Department of Fibrosis, Inflammation and Remodelling in Renal and Respiratory Diseases, FIRE, Paris, France.
Abstract
Objective: This study aimed to determine whether sCD163, a soluble macrophage marker up-regulated in numerous inflammatory disorders, is predictive of accelerated atherosclerosis associated with systemic lupus erythematosus (SLE). Methods: Carotid ultrasound was prospectively performed, at baseline and during follow-up, in 63 consecutive SLE patients asymptomatic for cardiovascular disease (CVD) and 18 volunteer health workers. Serum sCD163 level was determined at baseline using enzyme-linked immunosorbent assay. The primary outcome was the presence of a carotid plaque. Factors associated with carotid plaques were identified through multivariate analysis. Results: Despite a low risk for cardiovascular events according to Framingham score in both groups (2.1 ± 3.8% in SLE vs 2.1 ± 2.9% in controls; p = 0.416), ultrasound at baseline showed a carotid plaque in 23 SLE patients (36.5%) and two controls (11.1%) (p = 0.039). Multivariate analysis showed that SLE status increased the risk for carotid plaque by a factor of 9 (p = 0.017). In SLE patients, sCD163 level was high (483.7 ± 260.8 ng/mL vs 282.1 ± 97.5 ng/mL in controls; p < 0.001) and independently associated with carotid plaques, as assessed by stratification based on sCD163 quartile values (p = 0.009), receiver operating characteristics (p = 0.001), and multivariate analysis (p = 0.015). sCD163 at baseline was associated with the onset of carotid plaque during follow-up (3 ± 1.4 years) in SLE patients who had no carotid plaque at the first evaluation (p = 0.041). Conclusion: sCD163 is associated with progressing carotid plaque in SLE and may be a useful biomarker for accelerated atherosclerosis in SLE patients at apparent low risk for CVD.
Objective: This study aimed to determine whether sCD163, a soluble macrophage marker up-regulated in numerous inflammatory disorders, is predictive of accelerated atherosclerosis associated with systemic lupus erythematosus (SLE). Methods: Carotid ultrasound was prospectively performed, at baseline and during follow-up, in 63 consecutive SLEpatients asymptomatic for cardiovascular disease (CVD) and 18 volunteer health workers. Serum sCD163 level was determined at baseline using enzyme-linked immunosorbent assay. The primary outcome was the presence of a carotid plaque. Factors associated with carotid plaques were identified through multivariate analysis. Results: Despite a low risk for cardiovascular events according to Framingham score in both groups (2.1 ± 3.8% in SLE vs 2.1 ± 2.9% in controls; p = 0.416), ultrasound at baseline showed a carotid plaque in 23 SLEpatients (36.5%) and two controls (11.1%) (p = 0.039). Multivariate analysis showed that SLE status increased the risk for carotid plaque by a factor of 9 (p = 0.017). In SLEpatients, sCD163 level was high (483.7 ± 260.8 ng/mL vs 282.1 ± 97.5 ng/mL in controls; p < 0.001) and independently associated with carotid plaques, as assessed by stratification based on sCD163 quartile values (p = 0.009), receiver operating characteristics (p = 0.001), and multivariate analysis (p = 0.015). sCD163 at baseline was associated with the onset of carotid plaque during follow-up (3 ± 1.4 years) in SLEpatients who had no carotid plaque at the first evaluation (p = 0.041). Conclusion: sCD163 is associated with progressing carotid plaque in SLE and may be a useful biomarker for accelerated atherosclerosis in SLEpatients at apparent low risk for CVD.
Authors: Anna Dieden; Leone Malan; Catharina M C Mels; Leandi Lammertyn; Annemarie Wentzel; Peter M Nilsson; Petri Gudmundsson; Amra Jujic; Martin Magnusson Journal: Medicine (Baltimore) Date: 2021-05-21 Impact factor: 1.817