Thematic stream: co-morbidity.

Background: Tumor necrosis factor alpha (TNFα) may act as a link between inflammation and cardiovascular disease through several effects including the induction of insulin resistance (IR). The purpose of this study was to clarify if long-term modulation of inflammatory activity by TNFα inhibitors in RA patients has some influence on insulin sensitivity.Methods: Sixteen RA patients treated with anti-TNFα agents were followed during one year. Disease activity was assessed by DAS28, IR was determined by using Homeostatic Model Assessment-2, body composition was evaluated by impedance analysis, physical activity by accelerometry, abdominal fat distribution by magnetic resonance imaging, and serum level of key adipokines were quantified by ELISA.Results: Body mass indices were increased significantly after one year (25.71±3.20 vs 28.06±4.57 kg/m2, p=0.02) of treatment. Body composition interms of fat and fat-free mass had not changed except for a significant elevation of body cell mass (25.50±4.60 vs 26.60±3.17 kg, p=0.02). Values of visceral intraabdominal and subcutaneous abdominal adipose tissue were not modified. Levels of IR, beta cell production or insulin sensitivity did not change along the study. Basal levels of adiponectin, visfatin, leptin, ghrelin, resistin, and apelin did not change in response to anti-TNFα treatment; only retinol binding protein 4 showed a significant change (51.7±32.7 vs 64.9±28.4 μg/mL, p=0.03) at the end of the study.Conclusions: Insulin resistance, adiposity distribution, body composition, andserum levels of adipokines are not significantly affected by long-term inhibitionof TNFα in RA patients. Our findings question the suggested beneficial role ofanti-TNFα treatments in insulin resistance. [ABSTRACT FROM AUTHOR]