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Background In general population,a high body mass index,is considered protective against osteoporosis.The relationship of body composition and abdominal adiposity with bone mineral density (BMD) in rheumatoid arthritis (RA) has not been explored. Objectives To study if body composition and abdominal adiposity are related to BMD in RA. Methods 197 women (100 RA, 97 controls) adjusted for age and comorbidity were recruited. We determine: body mass index, waist circumference, bone mass by DEXA of the hip, lumbar spine, total body; lean and fat mass according to specific rates and locations; sarcopenia patterns, levels of vitamin D and osteoprotegerin, as well as abdominal fat by MRI, in both groups. Multivariate analysis was performed to study the relationship between bone mass and patterns of body composition and with abdominal adiposity. Results RA patients showed lower levels of lumbar bone values (βcoef. gr/cm2 -64 [95% CI -122 to 6], p=0.03) and a lower percentage of total body bone mass (βcoef -0.3% [95% CI, 0.5 to 0.1], p=0.01) after adjustment for age and comorbidity. Although values tended to be lower in RA in other areas such as femoral neck, total hip, Ward's triangle or femoral shaft, these differences were not statistically significant. Patients tended to have higher frequency of obesity as BMI>30 kg/m2 (43% vs. 31%, p=0.09), although the analysis of body compartments, fat and lean mass rates, as well as abdominal adiposity, showed no difference between patients and controls. Fat and lean masses were associated,in a positive way, with the levels of BMD at all sites in both groups (total hip β coef. Tscore 1.15 [95% CI 0.08- 0.24], p=0.00 in RA and β coef T score 0.16 [95% CI 0.07-0.24], p=0.00) in controls, after adjusting for age, comorbidity, and vitamin D levels and osteoprotegerin. The values of parietal abdominal adiposity showed a positive relationship with the values of total hip T score in both controls (0.04 T score β coef. [95% CI 0.01 to 0.07], p=0.01) and patients (0.05 T β coef. score [95% CI 0.02-0.07], p=0.00).This relationship was not found with the values of visceral abdominal adiposity. The presence of sarcopenia phenotype tended to be higher in patients (OR 2.95 [95% CI 0.93 to 9.29], p=0.06]. This sarcopenia was associated with lower BMD at the total hip (β coef. T score -1.90 [95% CI, 3.61-0.20], p=0.03) after adjustment for disease activity scores, age, ESR, CRP, rheumatoid factor and vitamin D and osteoprotegerin levels. In contrast, the presence of sarcopenia had no influence on bone mass in controls. Similarly, the combination of obesity and sarcopenia (sarcopenic obesity) showed no association with bone mass in either groups. Conclusions The protective role of fat and lean mass on BMD is preserved in patients. The pattern of sarcopenia, after adjusting for disease activity was associated with low bone mass in RA. This suggests an independent role of this sarcopenia on bone density in RA, but not in healthy subjects. Disclosure of Interest None declared DOI 10.1136/...

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Objectives It has been suggested that resistance to insulin action is a feature that accompanies rheumatoid arthritis (RA), a disease where chronic inflammation predominates and classical triggers for insulin resistance (IR) like obesity and diabetes are absents. However, data regarding characterization of RA features associated with this insulin resistance (IR) are lacking. The aim of this study was to investigate how sensitivity to insulin and markers of beta cell dysfunction (proinsulin processing metabolites) are expressed in RA. Methods 101 non-diabetic RA patients and 99 non-diabetic sex and age-matched controls were included in this study. Insulin sensitivity function through homeostatic model assessment (HOMA2), and beta cell secretion through insulin, split and intact proinsulin, and C-peptide were assessed in both groups. We performed multiple regression analysis to compare IR between groups and to explore the relation between RA features and IR. Data were adjusted for glucocorticoids intake and for IR classical risk factors. Results RA patients compared to controls show higher HOMA-IR (logHOMA-IR, beta coefficient, 0.40 [95% CI 0.20-0.59], p=0.00). When this data was adjusted for glucocorticoids intake, non-on corticosteroid patients maintained a higher IR index (beta coef. 0.14 [95% CI 0.05-0.24], p=0.00). Current prednisone treatment was not associated with higher IR in the patients’ intragroup comparison (beta coef. 0.56 [1.13-1.19], p=0.22). Insulin processing signaling in RA patients showed impaired features via an elevated intact proinsulin levels (beta coef. 3.13 [0.81-5.44] pMol/L, p=0.03 for the comparison between patients and controls). Split proinsulin levels were also higher in RA patients (beta coef. 13.7 pmol/L [3.57-9.40], p=0.00) even adjusting for prednisone intake (beta coef. 2.66 pmol/L [95%CI 1.62-5.95] for non steroids RA patients when compared to controls). In multiple regression analysis, RA features (disease duration, rheumatoid factor, erythrocyte sedimentation rate, C-reactive protein, disease activity through HAQ and DAS28 scores, and current non-biologic disease modifying antirheumatic drug), when adjusted for sex, age and body mass index, were not associated with IR or insulin propeptides. Conclusions Beta cell signaling is impaired in non-diabetic and non-corticoids RA patients. Disclosure of Interest None Declared

Objectives Rheumatoid Arthritis (RA) patients show alterations in cholesterol and lypoproteins levels. These disturbances seem to be related to the inflammation that takes place in the disease, but the pathological mechanisms that leed to it are unknown. Cholesterol ester transfer protein (CETP) is an enzyme that allows transference of cholesterol ester from HDL to LDL-cholesterol particles. CETP has recently gained interest as therapeutic goal of new treatments developed to treat dyslipidemia. The aim of this study is to describe the role of this enzyme in a model of chronic inflammation associated dyslipidemia as it occurs in rheumatoid arthritis. Methods 101 RA patients and 115 sex and age-matched controls were included. Serum levels of CEPT were measured by an enzimelinked inmunoassay and the enzymatic activity by a specific kit (Roar CEPT activity assay kit). In both patients and controls classical lipidic profile (cholesterol, triglycerides, HDL and LDL cholesterol, apolipoprotein A1, apolipoprotein B and lipoprotein A) was defined. Also ESR and CRP were determined. In RA patients disease activity indexes like DAS28 and HAQ were collected, as well as, sociodemographic variables, comorbidility and anthropometric variables. Multivariate analysis was performed to compare results between patients and controls adjusting for corticosteroids intake and for classical dyslipidemia risk factors. Results Serum protein levels were correlated with the enzimatic activity (r=0,5, p=0,00), showing that serum levels could be enough to express the activity of this enzime. Patients show lower CETP activity levels after adjusting for sex and age (beta coefficient -0,52 pmol/l, CI95% -0,87–0,18, p=0,01). In patients, CRP levels show a negative correlation with CETP activity (r=-0.34, p=0,03); in controls this correlation did not achieve the stadistic significance. Disease activity scores like DAS28 did not show association with CETP. Conclusions CETP is underexpressed in RA patients. Differencial characteristics of dyslipIdemia in RA could be partly explained by this fact. Disclosure of Interest None Declared