Hiurma Sánchez-Pérez1, Juan Carlos Quevedo-Abeledo2, Laura de Armas-Rillo3, Íñigo Rua-Figueroa2, Beatriz Tejera-Segura4, Estefanía Armas-González5, José David Machado6, Jose A García-Dopico7, Alejandro Jimenez-Sosa8, Carlos Rodríguez-Lozano2, Federico Díaz-González1,9, Miguel A González-Gay10,11,12, Iván Ferraz-Amaro1. 1. Division of Rheumatology, Hospital Universitario de Canarias, Tenerife. 2. Division of Rheumatology, Hospital Doctor Negrín, Las Palmas de Gran Canaria. 3. Universidad Europea de Canarias, Tenerife. 4. Division of Rheumatology, Hospital Insular de Gran Canaria, Las Palmas de Gran Canaria. 5. Department of Biochemistry, Microbiology, Cell Biology and Genetics. 6. Department of Pharmacology, Faculty of Medicine, Universidad de La Laguna. 7. Division of Central Laboratory. 8. Research Unit, Hospital Universitario de Canarias, Tenerife. 9. Department of Internal Medicine, Faculty of Medicine, Universidad de La Laguna, La Laguna. 10. Division of Rheumatology, Hospital Universitario Marqués de Valdecilla, Universidad de Cantabria. 11. Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Hospital Universitario Marqués de Valdecilla, IDIVAL, Santander, Spain. 12. Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa.
Abstract
OBJECTIVES: Lipid profiles appear to be altered in SLE patients due to disease activity and inflammation. Cholesterol efflux capacity (CEC) is the ability of high-density lipoprotein cholesterol to accept cholesterol from macrophages. CEC has been linked to cardiovascular events in the general population and is impaired in SLE patients. The aim of this study was to establish whether CEC is related to subclinical carotid atherosclerosis in SLE patients. METHODS: The present report is of a cross-sectional study that encompassed 418 individuals: 195 SLE patients and 223 controls. CEC, using an in vitro assay, and lipoprotein serum concentrations were assessed in patients and controls. Carotid intima-media thickness and carotid plaques were evaluated in SLE patients. A multivariable analysis was performed to study the relationship of CEC to SLE-related data, lipid profile and subclinical carotid atherosclerosis. RESULTS: CEC was downregulated in SLE patients [8.1 (4.2) % vs 16.9 (10.4) %, P = 0.004). This occurred independently of traditional cardiovascular risk factors, statin use or other variations in the lipid profile related to the disease. Traditional cardiovascular risk factors, both in patients and controls, and SLE-related data such as activity, severity or damage were not associated with CEC. After multivariable regression analysis including lipid profile-related molecules, CEC was inversely and independently associated with the presence of carotid plaques in SLE patients [odds ratio 0.87 (95% CI: 0.78, 0.97), P = 0.014]. CONCLUSION: CEC is impaired in SLE patients independently of other inflammation-related lipid profile modifications that occur during the disease. CEC is associated with carotid plaques in SLE patients.
OBJECTIVES:Lipid profiles appear to be altered in SLEpatients due to disease activity and inflammation. Cholesterol efflux capacity (CEC) is the ability of high-density lipoprotein cholesterol to accept cholesterol from macrophages. CEC has been linked to cardiovascular events in the general population and is impaired in SLEpatients. The aim of this study was to establish whether CEC is related to subclinical carotid atherosclerosis in SLEpatients. METHODS: The present report is of a cross-sectional study that encompassed 418 individuals: 195 SLEpatients and 223 controls. CEC, using an in vitro assay, and lipoprotein serum concentrations were assessed in patients and controls. Carotid intima-media thickness and carotid plaques were evaluated in SLEpatients. A multivariable analysis was performed to study the relationship of CEC to SLE-related data, lipid profile and subclinical carotid atherosclerosis. RESULTS: CEC was downregulated in SLEpatients [8.1 (4.2) % vs 16.9 (10.4) %, P = 0.004). This occurred independently of traditional cardiovascular risk factors, statin use or other variations in the lipid profile related to the disease. Traditional cardiovascular risk factors, both in patients and controls, and SLE-related data such as activity, severity or damage were not associated with CEC. After multivariable regression analysis including lipid profile-related molecules, CEC was inversely and independently associated with the presence of carotid plaques in SLEpatients [odds ratio 0.87 (95% CI: 0.78, 0.97), P = 0.014]. CONCLUSION: CEC is impaired in SLEpatients independently of other inflammation-related lipid profile modifications that occur during the disease. CEC is associated with carotid plaques in SLEpatients.
Authors: Alejandro Hernández-Camba; Marta Carrillo-Palau; Laura Ramos; Laura de Armas-Rillo; Milagros Vela; Laura Arranz; Miguel Á González-Gay; Iván Ferraz-Amaro Journal: Clin Transl Gastroenterol Date: 2022-06-01 Impact factor: 4.396
Authors: Hiurma Sánchez-Pérez; Juan C Quevedo-Abeledo; Beatriz Tejera-Segura; Laura de Armas-Rillo; Iñigo Rúa-Figueroa; Miguel A González-Gay; Iván Ferraz-Amaro Journal: Ther Adv Musculoskelet Dis Date: 2020-11-28 Impact factor: 5.346
Authors: Juan Carlos Quevedo-Abeledo; Candelaria Martín-González; Carmen Ferrer-Moure; Laura de Armas-Rillo; Maria Vanesa Hernandez-Hernandez; Miguel Á González-Gay; Iván Ferraz-Amaro Journal: Front Immunol Date: 2022-05-09 Impact factor: 8.786
Authors: Candelaria Martín-González; Carmen Ferrer-Moure; Miguel Á González-Gay; Iván Ferraz-Amaro; Juan Carlos Quevedo-Abeledo; Antonia de Vera-González; Alejandra González-Delgado; Julio Sánchez-Martín Journal: Arthritis Res Ther Date: 2022-05-10 Impact factor: 5.606
Authors: Juan Carlos Quevedo-Abeledo; Miguel Á González-Gay; Iván Ferraz-Amaro Journal: Ther Adv Musculoskelet Dis Date: 2022-04-19 Impact factor: 3.625