E F Borba1, E Bonfá. 1. Division of Rheumatology, São Paulo University Medical School Hospital, Brazil.
Abstract
OBJECTIVE: To determine the influence of systemic lupus erythematosus (SLE), disease activity, and anticardiolipin antibodies (aCL) on lipid profile, in order to identify patients with high risk for coronary artery disease (CAD). METHODS: Fasting lipid profiles were performed in 36 consecutive female SLE patients without any therapy and 30 controls. Exclusion criteria were diabetes mellitus, CAD, liver or thyroid disease, ingestion of lipid-raising drugs, serum creatinine > or = 1.5 mg/dl, and proteinuria > or = 0.5 g/d. Disease activity was measured by SLEDAI. RESULTS: High levels of VLDL-C and TG and low levels of HDL-C, the 'lupus pattern', were observed in inactive SLE compared to controls (P < 0.05). Active disease enhanced this difference inducing a more striking increase in VLDL-C and TG levels and also a decrease in HDL-C and LDL-C levels compared to inactive SLE patients (P < 0.05), characterizing the 'active lupus pattern'. Moreover, a significant correlation was found between SLEDAI scores and all lipid fractions. Furthermore these lipid abnormalities were particularly associated with vasculitis. Lower HDL-C levels detected in IgG aCL+ patients compared to IgG aCL- patients were not confirmed by two-way analysis of variance which demonstrated that this difference was exclusively caused by disease activity. CONCLUSIONS: Our findings suggest that SLE patients have a lipid profile abnormality which is aggravated by disease activity and may reside in a defect of VLDL metabolism. This pattern of dyslipoproteinemia may increase the risk of developing coronary artery disease.
OBJECTIVE: To determine the influence of systemic lupus erythematosus (SLE), disease activity, and anticardiolipin antibodies (aCL) on lipid profile, in order to identify patients with high risk for coronary artery disease (CAD). METHODS: Fasting lipid profiles were performed in 36 consecutive female SLEpatients without any therapy and 30 controls. Exclusion criteria were diabetes mellitus, CAD, liver or thyroid disease, ingestion of lipid-raising drugs, serum creatinine > or = 1.5 mg/dl, and proteinuria > or = 0.5 g/d. Disease activity was measured by SLEDAI. RESULTS: High levels of VLDL-C and TG and low levels of HDL-C, the 'lupus pattern', were observed in inactive SLE compared to controls (P < 0.05). Active disease enhanced this difference inducing a more striking increase in VLDL-C and TG levels and also a decrease in HDL-C and LDL-C levels compared to inactive SLEpatients (P < 0.05), characterizing the 'active lupus pattern'. Moreover, a significant correlation was found between SLEDAI scores and all lipid fractions. Furthermore these lipid abnormalities were particularly associated with vasculitis. Lower HDL-C levels detected in IgG aCL+ patients compared to IgG aCL- patients were not confirmed by two-way analysis of variance which demonstrated that this difference was exclusively caused by disease activity. CONCLUSIONS: Our findings suggest that SLEpatients have a lipid profile abnormality which is aggravated by disease activity and may reside in a defect of VLDL metabolism. This pattern of dyslipoproteinemia may increase the risk of developing coronary artery disease.
Authors: Elena Schiopu; Karen M Au; Maureen A McMahon; Mariana J Kaplan; Anagha Divekar; Ram R Singh; Daniel E Furst; Philip J Clements; Nagesh Ragvendra; Wenpu Zhao; Paul Maranian; Dinesh Khanna Journal: Rheumatology (Oxford) Date: 2013-12-19 Impact factor: 7.580