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Inflammatory Mechanisms Affecting the Lipid Profile in Patients with Systemic Lupus Erythematosus

CECILIA P. CHUNG, ANNETTE OESER, JOSEPH SOLUS, INGRID AVALOS, TEBEB GEBRETSADIK, AYUMI SHINTANI, MacRAE F. LINTON, SERGIO FAZIO, and C. MICHAEL STEIN

ABSTRACT.

Objective. Increased low density lipoprotein (LDL) cholesterol and triglycerides, and decreased high density lipoprotein (HDL) cholesterol concentrations are associated with adverse cardiovascular risk in the general population. Patients with systemic lupus erythematosus (SLE) have an altered lipid profile characterized by increased triglycerides and decreased HDL cholesterol concentrations. We examined the relationships between lipid concentrations, cytokines, and inflammatory markers in patients with SLE.

Methods. Fasting lipid concentrations, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR) were measured in 110 patients with SLE. Disease activity was quantified by the SLE Disease Activity Index (SLEDAI), and disease damage by the Systemic Lupus International Collaborating Clinics (SLICC) score. Concentrations of circulating tumor necrosis factor-a (TNF-a), interleukin 6 (IL-6), and insulin were measured and insulin sensitivity calculated.

Results. Lower concentrations of HDL cholesterol were independently associated with higher ESR (p < 0.001), IL-6 (p = 0.02), SLEDAI (p = 0.04), and TNF-a (p = 0.04) after adjustment for age, sex, race, body mass index, insulin sensitivity, and current use of corticosteroids or hydroxychloroquine. Triglyceride concentrations were associated with higher CRP concentrations (p = 0.02) and SLICC score (p = 0.04).

Conclusion. Deleterious changes in lipid profile are independently associated with higher concentrations of markers and mediators of inflammation and disease activity and damage in patients with SLE. (First Release July 15 2007; J Rheumatol 2007;34:1849-54)

Key Indexing Terms:

CHOLESTEROL
TRIGLYCERIDES
CYTOKINES
SYSTEMIC LUPUS ERYTHEMATOSUS
INFLAMMATION

From the Departments of Medicine, Molecular Physiology and Biophysics, Biostatistics, Pathology, and Pharmacology, Vanderbilt University, Nashville, Tennessee, USA.

Supported by grants HL04012, HL65082, and GM5M01-RR00095 from the National Institutes of Health and by a grant from the Lupus Foundation of America, Nashville Chapter. Dr. Avalos is supported in part by a grant from the American College of Rheumatology.

C.P. Chung, MD, MPH; A. Oeser, BS; I. Avalos, MD, Department of Medicine; M.F. Linton, MD; C.M. Stein, MD, Departments of Medicine and Pharmacology; S. Fazio, MD, PhD, Departments of Medicine and Pathology; J. Solus, PhD, Departments of Molecular Physiology and Biophysics and Pharmacology; T. Gebretsadik, MPH; A. Shintani, MPH, PhD, Department of Biostatistics, Vanderbilt University.

Address reprint requests to Dr. C.P. Chung, Rheumatology Division, Vanderbilt University School of Medicine, T-3219 MCN, 1161 21st Ave., Nashville, TN 37232, USA. E-mail: c.chung@vanderbilt.edu

Accepted for publication April 25, 2007.