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Association of circulating interleukin‐18 levels with cardiovascular risk factors in patients with systemic lupus erythematosus
Author(s) -
Tso Tim K,
Huang WenNan,
Huang HuiYu
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a185-b
Subject(s) - medicine , insulin resistance , proinflammatory cytokine , triglyceride , homocysteine , endocrinology , pathogenesis , immunology , confounding , body mass index , metabolic syndrome , insulin , obesity , inflammation , cholesterol
Objective Systemic lupus erythematosus (SLE) is associated with premature atherosclerosis. Recent studies indicated that the concentrations of circulating interleukin (IL)‐18, a novel proinflammatory Th1 cytokine, in SLE patients were significantly higher than those in healthy subjects. The objective of this study was to examine the relationship between plasma IL‐18 levels and cardiovascular risk factors in SLE patients. Method Both traditional and nontraditional cardiovascular risk factors were determined in a total of 70 female SLE patients. All patients were further classified into subgroups based on the tertiles of plasma IL‐18 levels determined by enzyme‐linked immunosorbent assay. Results SLE patients with IL‐18 levels in the top tertile compared with bottom tertile had significantly higher plasma levels of insulin, triglyceride (TG), homocysteine, and values for homeostasis model assessment insulin resistance (HOMA IR) and HOMA β‐cell. In addition, plasma levels of IL‐18 correlated positively and significantly with insulin, TG, homocysteine, body mass index, diastolic blood pressure, HOMA IR, HOMA β‐cell, and brachial‐ankle pulse wave velocity in all SLE patients. Conclusion Elevated IL‐18 levels are associated with certain cardiovascular risk factors in SLE patients. This proinflammatory cytokine along with markers for lipid abnormality, insulin resistance and vascular damage could involve in the cardiovascular pathogenesis in SLE.