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    Role of insulin resistance in increased frequency of atherosclerosis detected by carotid ultrasonography in rheumatoid arthritis
    (J Rheumatol Publ Co, 2006) Pamuk, Omer Nuri; Unlu, Ercument; Çakir, Necati
    Objective. We evaluated the presence of subclinical atherosclerosis and factors influencing atherosclerosis, including insulin resistance (IR), in patients with rheumatoid arthritis (RA). Methods. Sixty-three patients with RA and 34 controls were studied. Patients' cardiovascular risk factors were recorded; biochemical variables were determined. Intima-media thickness (IMT) of carotid arteries was determined by B-mode ultrasonography, and presence of atheromatous plaques was determined. IR was calculated according to the HOMA-IR homeostasis model. Results. There were no differences in atherosclerotic risk factors between patients with RA and controls. In the RA group, the median carotid IMT was 0.61 mm (range 0.56-0.74), greater than the 0.54 mm (range 0.50-0.64) in controls (p = 0.01). There was a tendency to a higher frequency of carotid plaques in the RA group compared to controls [12 RA patients (19%) vs 2 controls (5.9%); p = 0.10]. Multivariate regression analysis revealed the factors that had an independent effect on increased carotid IMT: age (p < 0.001), male sex (p = 0.01), and total cholesterol level (p=0.02). In RA patients with plaques, age (64.5 vs 48 yrs; p = 0.005), carotid IMT (0.75 vs 0.60 mm; p 0.001), frequency of hypertension (58.3% vs 23.5%; p = 0.03), and IR (83.3% vs 29.4%; p = 0.001) were higher. Multivariate logistic regression analysis showed that factors independently associated with the presence of plaques were IR (OR 15.85, 95% CI 2.23-112.89, p = 0.006) and age (OR 1.11, 95% CI 1.02-1.21, p = 0.02). In RA patients, HOMA-IR correlated with age (r = 0.26, p = 0.04), Health Assessment Questionnaire score (r = 0.28, p = 0.04), and concentrations of triglyceride (r = 0.39, p = 0.003) and cholesterol (r = 0.33, p = 0.02). Conclusion. IR in the setting of active rheumatoid disease may contribute to mechanisms of accelerated atherogenesis observed in patients with RA.