Background: The metabolic syndrome is an independent risk factor for ischaemic heart disease. Patients with systemic lupus erythematosus (SLE) have accelerated atherosclerosis; however, there are no controlled studies of the metabolic syndrome in patients with SLE.
Objective: To compare the prevalence of the metabolic syndrome in patients with SLE and controls and to evaluate its relationship to other cardiovascular risk factors and inflammation.
Methods: 102 patients with SLE and 101 controls were studied. The prevalence of the metabolic syndrome was compared in patients and controls using the National Cholesterol Education Program Adult Treatment Panel III (NCEP) and the World Health Organization (WHO) definitions, and associations with cardiovascular risk factors and lupus characteristics were examined.
Results: The metabolic syndrome was present in 32.4% of patients and in 10.9% of controls subjects (p<0.001) using the WHO definition that requires direct determination of insulin resistance, and in 29.4% of patients with SLE and in 19.8% of controls (p = 0.14) using the NCEP definition. Among patients with SLE, both definitions were significantly associated with higher concentrations of C reactive protein (p = 0.001) and the NCEP definition was significantly associated with higher concentrations of homocysteine (p<0.001), lipoprotein (a) (p = 0.02) and cholesterol (p = 0.04). Neither lupus disease activity nor damage scores were associated with the metabolic syndrome.
Conclusions: Patients with SLE have a higher prevalence of insulin resistance and consequently of the WHO-defined metabolic syndrome than controls. In patients with SLE, the metabolic syndrome was associated with higher levels of inflammation and may provide a link between inflammation and increased cardiovascular risk.
- BMI, body mass index
- CRP, C reactive protein
- HDL, high-density lipoprotein
- HOMA, homeostasis model assessment
- LDL, low-density lipoprotein
- NCEP, National Cholesterol Education Program Adult Treatment Panel III
- SLE, systemic lupus erythematosus
- WHO, World Health Organization
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Published Online First 10 August 2006
Funding: This study was supported by grants (HL04012, HL65082 and GM5M01-RR00095) from the National Institutes of Health and by grants from the Lupus Foundation of America, Nashville Chapter and the Lupus Clinical Trials Consortium. IA is funded in part by a grant from the American College of Rheumatology
Competing interests: CPC received a CHORD (Centocor Health Outcomes in Rheumatic Diseases) Fellowship in 2004, grants: HL065082, HL067964, 3U18 HS010384-07S1, HHSA290200500421. IA, ACR REF 2006 Fellowship award. AO, TG, AS, no disclosures. In PR’s opinion, this is not relevant to the paper submitted but in the interest of full disclosure is declared: Honoraria (Genzyme). CMS, grants RO1 HL65082, 5K24 HL04012-05, 5RO1-HL67964, 2U01 HL65962-03, 5P01 GM31304-21, 5U18 HS010384-07, 1RO1 HL081707-01, Lupus Foundation, 5 RO1 HL65082-03. In CMS’s opinion, these are not relevant to the paper submitted but in the interest of full disclosure are declared. Consultant fees from Bristol Myers Squibb for preparation of a series of lectures on trial design; royalty fees from the publication of textbooks of rheumatology; fees from medicolegal chart review in two cases of drug toxicity; an honorarium from the American Society of Clinical Pharmacology and Therapeutics for editing their journal; fees from the NIH for participating in peer review. CMS holds a patent on the use of IL2 to monitor ciclosporine activity—the patent has yielded no income.
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