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  • Title: The acute phase response does not fully predict the presence of insulin resistance and dyslipidemia in inflammatory arthritis.
    Author: Dessein PH, Joffe BI, Stanwix A, Botha AS, Moomal Z.
    Journal: J Rheumatol; 2002 Mar; 29(3):462-6. PubMed ID: 11908557.
    Abstract:
    OBJECTIVE: Rheumatoid arthritis (RA) is associated with an increased mortality rate from cardiovascular disease. This may relate to insulin resistance and dyslipidemia, which were both reported to correlate with the acute phase response in RA. We investigated whether insulin resistance and dyslipidemia could be explained by the acute phase response as well as excess weight in inflammatory arthritis. METHODS: We investigated 87 patients, 38 with RA, 29 with spondyloarthropathy, 20 with undifferentiated inflammatory arthritis. Thirty age, sex, and race matched healthy volunteers served as controls. Fasting blood samples were taken for determination of erythrocyte sedimentation rate (ESR), plasma glucose, serum insulin, and total cholesterol (chol), low density lipoprotein cholesterol (LDL-chol), high density lipoprotein cholesterol (HDL-chol), and triglycerides. Insulin resistance was estimated by the homeostasis model assessment for insulin resistance (HOMA) and the quantitative insulin sensitivity check index (QUICKI). RESULTS: In controls the mean (SD) HOMA (microU x mmol/ml x l), QUICKI, body mass index (BMI, kg/m2), and ESR (mm/h) were 1.1 (0.5), 0.393 (0.048), 22.9 (2.8), and 13 (8) in patients; they were 1.9 (1.3), 0.357 (0.037), 26.5 (4.2), and 26 (18) in controls, respectively. Each of these differences was highly significant (p < 0.001). HDL-chol concentrations were lower (p = 0.002) and chol/HDL-chol ratios and triglyceride levels were higher (p < 0.001 and p = 0.004, respectively) in patients compared to controls. A high ESR predicted insulin resistance and dyslipidemia, while a high BMI similarly predicted insulin resistance but not dyslipidemia. After controlling for ESR and BMI, insulin sensitivity was no longer different between patients and controls, while HDL-chol concentrations remained lower (p = 0.015) and chol/HDL-chol ratios remained higher (p = 0.003) in patients compared to controls. CONCLUSION: Insulin resistance and dyslipidemia were highly prevalent in patients with inflammatory arthritis. The acute phase response and excess weight could fully explain the insulin resistance but only partially explain the dyslipidemia. These findings have important implications for the management of inflammatory arthritis.
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