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Objectives. The aims of this study were to study physical activity (PA) in patients with RA by accelerometry and to determine to what degree their mobility is affected by disease activity.Methods. A group of 50 RA patients, without lower limb clinical disease, and 50 age- and sex-matched healthy controls were included in this cross-sectional study. PA was assessed by accelerometry and with the International Physical Activity Questionnaire (IPAQ). We performed multiple regression analysis not only to compare PA between groups, but also to explore the relation between RA features, including disease activity and cardiovascular risk parameters, and PA. In a randomized group of 30 RA patients a test–retest study was carried out in order to determine the correlation between variations in disease activity and PA.Results. The number of minutes of moderate and vigorous activity per day, as evaluated by accelerometry, was significantly lower in RA patients than in healthy controls. In RA patients, accelerometry and IPAQ demonstrated concordance to a moderate degree [quadratic weighed kappa index 0.27 (0.06–0.48), P = 0.02]. HAQ negatively correlated with both IPAQ and accelerometry data. The 28-joint DAS using CRP (DAS28-CRP) was also inversely related with IPAQ. Framingham score and metabolic syndrome were inversely associated with PA in RA patients. Interestingly, variations in PA by accelerometry inversely correlated with changes in RA disease activity (r = −0.42, P = 0.02).Conclusion. In RA patients, accelerometry is a reliable technique to evaluate PA. This study not only showed that RA patients spend less time doing moderate and vigorous PA than healthy controls, but also PA, as assessed by accelerometry, was sensitive to any changes in disease activity. [ABSTRACT FROM PUBLISHER]

Interleukin (IL) 1, and its family member, IL-1 receptor antagonist (IL-1ra), are involved in the pathogenesis and inflammation perpetuation of patients with rheumatoid arthritis (RA). Besides, IL-1 has been linked to an increased risk and greater severity of cardiovascular (CV) disease. We aimed to study if IL-1ra is related to the CV manifestations—including lipid pattern and insulin resistance or subclinical atherosclerosis—that accompanies the disease in a large series of patients with RA. Cross-sectional study that encompassed 430 patients with RA. Serum IL-1ra levels were assessed. A multivariable analysis was performed to analyze the relation of IL-1ra to subclinical carotid atherosclerosis, and to traditional CV factors including a complete lipid molecules profile and insulin resistance or beta cell function indices. Body mass index, abdominal circumference, and the presence of obesity were significantly and positively associated with circulating IL-1ra. Similarly, erythrocyte sedimentation rate, and disease activity scores were significantly related to higher IL-1ra serum levels after adjustment for confounders. Neither carotid intima-media thickness nor the presence of carotid plaque were associated with serum levels of IL-1ra. However, after multivariable analysis circulating IL-1ra was independently and positively associated with higher serum levels of total cholesterol, triglycerides, and apolipoproteins B and C-III. Similarly, IL-1ra was related to higher levels of beta-cell function in the univariable analysis, although, in this case, significance was lost after adjustment. Among patients with RA, IL-1ra is associated with both disease activity and several traditional CV risk factors such as obesity and the presence of higher lipid levels. Our findings suggest that IL-1ra can represent a link between the inflammation and the CV disease risk that are present in patients with RA. [ABSTRACT FROM AUTHOR]

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]

Cardiovascular (CV) disease is the main cause of mortality in axial spondyloarthritis (axSpA). CV risk is enhanced by dysregulation of adipokines. Low omentin levels were associated with metabolic dysfunction and CV disease in conditions different from axSpA. Accordingly, we evaluated the genetic and functional implication of omentin in CV risk and subclinical atherosclerosis in a cohort of 385 axSpA patients. Subclinical atherosclerosis was evaluated by carotid ultrasound. Omentin rs12409609, in linkage disequilibrium with a polymorphism associated with CV risk, was genotyped in 385 patients and 84 controls. Serum omentin levels were also determined. omentin mRNA expression was assessed in a subgroup of individuals. Serum and mRNA omentin levels were lower in axSpA compared to controls. Low serum omentin levels were related to male sex, obesity, inflammatory bowel disease (IBD) and high atherogenic index. rs12409609 minor allele was associated with low omentin mRNA expression in axSpA. No association was observed with subclinical atherosclerosis at the genetic or functional level. In conclusion, in our study low omentin serum levels were associated with CV risk factors in axSpA. Furthermore, rs12409609 minor allele may be downregulating the expression of omentin. These data support a role of omentin as a CV risk biomarker in axSpA. [ABSTRACT FROM AUTHOR]

Objectives. The aim of this study was to confirm the implication of macrophage migration inhibitory factor (MIF) gene in SSc susceptibility or clinical phenotypes in a large European population.Methods. A total of 3800 SSc patients and 4282 healthy controls of white Caucasian ancestry from eight different European countries were included in the study. The MIF −173 single nucleotide polymorphism (SNP) was selected as genetic marker and genotyped using Taqman 5′ allelic discrimination assay.Results. The MIF −173 SNP showed association with SSc [P = 0.04, odds ratio (OR) = 1.10, 95% CI 1.00, 1.19]. Analysis of the MIF −173 polymorphism according to SSc clinical phenotype revealed that the frequency of the −173*C allele was significantly higher in the dcSSc group compared with controls (P = 5.30E-03, OR = 1.21, 95% CI 1.07, 1.38). Conversely, the frequency of the MIF −173*C allele was significantly underrepresented in the lcSSc group compared with dcSSc patients, supporting previous findings [(P = 0.04, OR = 0.86, 95% CI 0.75, 0.99); meta-analysis including previous results (P = 0.005, OR = 0.83, 95% CI 0.73, 0.94)].Conclusion. Our results confirm the role of MIF −173 promoter polymorphism in SSc, and provide evidence of a strong association with the dcSSc subgroup of patients. Hence, the MIF −173 variant is confirmed as a promising clinical phenotype genetic marker. [ABSTRACT FROM PUBLISHER]