A Fernández-Nebro1, J L Marenco2, F López-Longo3, M Galindo4, B E Hernández-Cruz5, J Narváez6, I Rúa-Figueroa7, E Raya-Alvarez8, A Zea9, M Freire10, A I Sánchez-Atrio11, R García-Vicuña12, J M Pego-Reigosa13, S Manrique-Arija14, L Nieves-Martín1, L Carreño3. 1. UGC Reumatología, Instituto de Investigación Biomédica de Málaga (IBIMA), Hospital Regional Universitario de Málaga/Universidad de Málaga, Málaga, Spain. 2. Hospital Virgen de Valme, Rheumatology Department, Sevilla, Spain. 3. Hospital General Universitario Gregorio Marañón, Rheumatology Department, Madrid, Spain. 4. Hospital Universitario 12 de Octubre, Rheumatology Department, Madrid, Spain. 5. Hospital Virgen Macarena, Rheumatology Department, Sevilla, Spain. 6. Hospital Universitario de Bellvitge, Rheumatology Department, Hospitalet de Llobregat, Barcelona, Spain. 7. Hospital Universitario de Gran Canaria Dr Negrín, Rheumatology Department, Las Palmas de Gran Canaria, Spain. 8. Hospital Clínico Universitario San Cecilio, Rheumatology Department, Granada, Spain. 9. Hospital Universitario Ramón y Cajal, Rheumatology Department, Madrid, Spain. 10. Complejo Hospitalario Universitario A Coruña, Rheumatology Department, A Coruña, Spain. 11. Hospital Universitario Príncipe de Asturias, Rheumatology Department, Alcalá de Henares, Madrid, Spain. 12. Hospital Universitario de la Princesa, Rheumatology Department, Madrid, Spain. 13. Complejo Hospitalario Universitario de Vigo, Rheumatology Department, Hospital del Mexoeiro, Instituto de Investigación Biomédica de Vigo (IBIV), Vigo, Spain. 14. UGC Reumatología, Instituto de Investigación Biomédica de Málaga (IBIMA), Hospital Regional Universitario de Málaga/Universidad de Málaga, Málaga, Spain sarama_82@hotmail.com.
Abstract
INTRODUCTION: Patients with systemic lupus erythematosus (SLE) have increased cardiovascular risk related to lipid changes induced by inflammatory activity, proteinuria and treatments. Our objective was to analyse lipid changes in a cohort of patients with SLE resistant to standard treatments who were treated with rituximab. METHODS: The study population comprised a retrospective multicentre, national cohort of patients with SLE resistant to standard treatments who were treated with rituximab. The basic lipid profile, concomitant treatment and disease activity were analysed at the start of the treatment, 24 weeks later, and at the end of the follow-up period. The effects of the main lupus variables and therapy on the lipid changes were analysed. RESULTS: Seventy-nine patients with active lupus treated with rituximab were assessed during 149.3 patient-years. Prior to the treatment, 69% had dyslipidaemia. The most frequent abnormalities were a low-density lipoprotein (LDL) level of ≥100 mg/dl (34%) and a high-density lipoprotein (HDL) level of <50 mg/dl (27%). Baseline total cholesterol (TC) and LDL levels correlated with the degree of proteinuria, while the concentration of triglycerides (TGs) correlated with the SLE Disease Activity Index (SLEDAI). TGs were reduced at short- and long-term follow-up after rituximab treatment. A multiple linear regression analysis identified that the reduction of the lupus inflammatory activity, particularly changes in proteinuria, was the only independent variable that was positively associated with the reduction in TGs after 24 weeks (p=0.001) and with TC (p=0.005) and TGs (p<0.001) at the end of the follow-up period. CONCLUSION: Our results suggest that rituximab may improve the long-term lipid profile of patients with SLE refractory to standard treatment, mainly by reducing inflammatory activity.
INTRODUCTION:Patients with systemic lupus erythematosus (SLE) have increased cardiovascular risk related to lipid changes induced by inflammatory activity, proteinuria and treatments. Our objective was to analyse lipid changes in a cohort of patients with SLE resistant to standard treatments who were treated with rituximab. METHODS: The study population comprised a retrospective multicentre, national cohort of patients with SLE resistant to standard treatments who were treated with rituximab. The basic lipid profile, concomitant treatment and disease activity were analysed at the start of the treatment, 24 weeks later, and at the end of the follow-up period. The effects of the main lupus variables and therapy on the lipid changes were analysed. RESULTS: Seventy-nine patients with active lupus treated with rituximab were assessed during 149.3 patient-years. Prior to the treatment, 69% had dyslipidaemia. The most frequent abnormalities were a low-density lipoprotein (LDL) level of ≥100 mg/dl (34%) and a high-density lipoprotein (HDL) level of <50 mg/dl (27%). Baseline total cholesterol (TC) and LDL levels correlated with the degree of proteinuria, while the concentration of triglycerides (TGs) correlated with the SLE Disease Activity Index (SLEDAI). TGs were reduced at short- and long-term follow-up after rituximab treatment. A multiple linear regression analysis identified that the reduction of the lupus inflammatory activity, particularly changes in proteinuria, was the only independent variable that was positively associated with the reduction in TGs after 24 weeks (p=0.001) and with TC (p=0.005) and TGs (p<0.001) at the end of the follow-up period. CONCLUSION: Our results suggest that rituximab may improve the long-term lipid profile of patients with SLE refractory to standard treatment, mainly by reducing inflammatory activity.