tbuckley/cabot-search huggingface dataset:
AB0815 Prevalence of dorsal and lumbar vertebral osteoarthritis in women over 50 years of age evaluated using the lane radiographic score in five latin-american countries
Authors: SM Carrillo, DX Xibillé, E Granados-Sandoval, D Curiel-Quiroz, E Denova-Gutierrez, MG Olvera-Soto, P Clark
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Osteoarthritis is the most common musculoskeletal disease worldwide. Spinal osteoarthritis (OA) is a frequent cause of back pain and disability in patients over 60. The frequency of radiographically-evident dorsal and lumbar OA in Latin America is unknown <h3>Objectives</h3> To determine the prevalence of dorsal and lumbar vertebral OA in a database-driven random sample of women 50 years of age and older from the Latin-American Vertebral Osteoporosis Study (LAVOS) in 5 LA countries (México, Brazil, Argentina, Colombia and Puerto Rico) <h3>Methods</h3> Lumbar and Dorsal X-rays were performed per a standardized protocol and analyzed independently by two trained radiologists and a general practitioner using the Lane score to establish diagnosis and degree of vertebral OA severity. Inter and intra observer agreement was determined to be k&gt;0.6. Descriptive statistics were used to analyze demographic variables. Prevalence was determined using means and standard deviations for quantitative variables and simple frequencies and percentages for qualitative variables. Bivariate analysis was performed to associate age, BMI and other variables with the presence of OA, using c<sup>2</sup> and the magnitude of association through OR and 95% CI, carrying out a multivariate analysis to adjust the frequency of OA to other variables <h3>Results</h3> 405 women, mean age 69.4 (58–80), median weight 64 kg (56.9–73.4) mean height 151.8 cm (±7.6) were analyzed. 5.65% were underweight, 21% had normal weight, 41.6% were overweight and 31.5% were obese. Argentina contributed 19% of the sample, Brazil 14.8%, Colombia 20.1%, México 33.3% and Puerto Rico 12.8%. OA prevalence per age group was 76.3% (95% CI 68.4–84.2) in those 50–59, 83.8% (95% CI76.6–91.2) in those 60–69, 84.3% (95% CI 76.7–91.7) in those 70–79 and 94.9% (95% CI 90.4–99.3) in those 80 or older (p=0.003). Prevalence per country was as follows: Brazil 93%, Colombia 90%, México 85%, Puerto Rico 79% and Argentina 74%. Prevalence per BMI was 80% in normal weight, 82.5% in overweight and 87.5% in obese. 72.6% of sampled women had dorsal OA (Argentina 48.1%, Brazil 65%, Puerto Rico 73.1%, México 79.3%, Colombia 90.1%). Obesity was a risk factor for the development of dorsal OA (OR 2.46) when compared to normal BMI (p=0.01). Lumbar OA was found in 44.9% of the sampled women (Argentina 68.8%, Brazil 65%, Colombia and Puerto Rico 42.3% each, México 37%). Adjusting for age, BMI, height loss, steroid use and physical activity, the OR for presenting OA is 6.45 (p&lt;0.001) in women over 80 compared to those 50–59 <h3>Conclusions</h3> Radiographic OA is highly prevalent in Latin American women over 50 and associated with progressing age and BMI. Brazil has the highest prevalence of OA. <h3>Disclosure of Interest</h3> None declared
FRI0573 Osteocytes are involved in the pathogenesis of osteoporosis in chronic cholestasis. effects of bilirubin and bile acids on osteocytic cell lines
Authors: S Ruiz-Gaspà, A Parés, A Combalia, P Peris, A Monegal, N Guañabens
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Mechanisms underlying osteoporosis in chronic cholestasis are complex and poorly understood. In this setting, osteoporosis mainly results from low bone formation, related to the effects of retained substances of cholestasis, such as bilirubin and bile acids. Thus, in "in vitro" studies, unconjugated bilirubin and serum from jaundiced patients decrease osteoblast viability, differentiation and mineralization. However, the influence of cholestasis on osteocytes, the most ubiquitous cells of the skeleton, is unknown. <h3>Objectives</h3> The aim of this study was to analyze the direct effects of increased molecules of cholestasis, such as bilirubin (Bil) and lithocholic acid (LCA), and the potential protective effect of ursodeoxycholic acid (UDCA) on the osteocytes. <h3>Methods</h3> MLO-Y4 and MLO-A5 osteocyte cell lines treated at different times and concentrations with Bil, LCA and UDCA were used to determine: 1) Viability: WST colorimetric method; 2) Differentiation: quantification of alkaline phosphatase (AP) activity; 3) Mineralization: Alizarin red staining quantification; and 4) Apoptosis: quantification of DNA fragmentation and caspase-3 activity. <h3>Results</h3> LCA (100μM) and Bil (50μM) significantly decreased viability in MLO-Y4 from 72 hours (10%) and 48 hours (11%), respectively (p≤0.01), and Bil decreased viability (49%) in MLO-A5 from 96 hours (p&lt;0.01). Bil decreased AP activity by 47% after 96 hours, under conditions of differentiation in MLO-Y4 (p≤0.01). There were no effects on AP activity in MLO-A5. After 14 days, Bil was associated with a significant mineralization decrease, as high as 87%, in MLO-A5 (p≤0.02). Moreover, Bil and LCA increased apoptosis in MLO-Y4, determined by DNA fragmentation (242% and 119%, respectively) and caspase-3 activity (190% and 251%, respectively) (p≤0.01) after 24 hours. In contrast, UDCA (100 μM) increased viability after 72 hours (11%) and decreased the deleterious effects of LCA or BiI (p≤0.02). UDCA increased AP activity in MLO-Y4 after 72 hours under growth conditions (p=0.018), and after 24 hours under differentiation conditions (p≤0.01). <h3>Conclusions</h3> Bilirubin and lithocholic acid have damaging effects on osteocytic cells decreasing viability, differentiation and mineralization, and increasing apoptosis, effects that are neutralized by the UDCA. These results indicate that substances retained in cholestasis impair osteocytic functions, and therefore may be involved in the pathogenesis of osteoporosis in cholestatic diseases. <h3>Disclosure of Interest</h3> None declared
THU0275 Importance of serum titers of antibodies against domain 1 of b2 glycoprotein 1
Authors: JA Gόmez-Puerta, T Urrego, A Hernández, S Ruiz Giraldo, C Rua, J Duque Botero, M Velázquez, AP Cadavid, AL Vanegas-García, CH Muñoz, LA González, G Vásquez
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> There is an increasing interest in the study of domain reactivity of antibodies against β2 glycoprotein I (anti-B2GPI) in patients with antiphospholipid syndrome (APS). Antibodies targeting domain 1 of the molecule (anti-D1) as the most relevant autoantibody subpopulation. Previous information of anti-D1 B2GPI comes from APS cohorts with Caucasian, Asian, and African-American patients. However, there are no studies in Mestizo and Afro-Latin American patients. <h3>Objectives</h3> Our aim was to evaluate the prevalence of Anti-D1 B2GPI antibodies in a cohort of Colombian patients with systemic lupus erythematosus (SLE) with and without thrombosis, primary APS and patients with previous history of recurrent miscarriages (RM) without APS criteria. <h3>Methods</h3> In this cross-sectional study we measured Anti-D1 B2GPI antibodies in a group of patients from Rheumatology Department, Coagulation clinic and Recurrent Pregnancy Loss Program at the Reproduction Group at Hospital San Vicente Fundaciόn and Universidad de Antioquia, respectively, at Medellín, Colombia. Anti-D1 B2GP1 antibodies were tested using a chemiluminescent immunoassay (QUANTA Flash B2GPI IgG, Inova Diagnostics). Mann-Whitney tests were used to compare data. <h3>Results</h3> One hundred and seventy seven (median age 33.5±12.1 years; 89% women) patients were included. One hundred thirty eight patients had SLE (78%), 27 primary APS (15%) and 13 RM (7%). Fifty five (31%) out of 177 patients had history of thrombosis and 41 (23%) of pregnancy losses. Overall, Anti-D1 B2GPI antibodies were positive (&gt;20 CU) in 35 (20%) of patients. Anti-D1 B2GPI were positive in 23%, 17% and 0% of patients with primary APS, SLE and RM, respectively. Overall, serum Anti-D1 B2GPI were significantly higher in patients with than without previous thrombosis (149.1±336.1 vs 16.3±61.8 CU, p&lt;0.0001) and in patients (SLE or primary APS) with previous history of pregnancy losses (40.2±123.1 vs 21.0±74.5 CU, p=0.04). Anti-D1 B2GPI were significantly higher in patients with primary APS vs SLE with thrombosis, and in patients with SLE with thrombosis vs SLE without thrombosis (Figure). No clinical associations were found among Anti-D1 B2GPI antibodies and other APS features. <h3>Conclusions</h3> Serum titers of Anti-D1 B2GPI antibodies were more than 9 times and 2 times higher in patients with thrombosis and pregnancy losses, respectively. In addition, serum titers were significantly higher in patients with primary APS than in SLE patients with thrombosis. Whether Anti D1- B2GPI antibodies titers are useful to differentiate patient with primary and secondary APS requires further analysis. <h3>Acknowledgements</h3> JA Gόmez-Puerta was supported by Colciencias (conv. 656 de 2014). Anti-D1 B2GPI antibodies were provided by Inova, Werfen, Colombia <h3>Disclosure of Interest</h3> None declared
AB0120 Accelerated osteogenic differentiation of human bone-derived cells in ankylosing spondylitis
Authors: Y-S Park, S Jo, I-H Sung, T-H Kim
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Ankylosing spondylitis (AS) is characterized by excessive bone formation with syndesmophytes, leading to bony ankylosis. The contribution of osteoblasts to the pathogenesis of ankylosis is poorly understood. <h3>Objectives</h3> The aim of this study was to determine molecular differences between disease controls (Ct) and AS bone-derived cells (BdCs) during osteogenic differentiation. <h3>Methods</h3> We confirmed osteoblastic differentiation of Ct and AS BdCs under osteogenic medium by observing morphological changes and measuring osteoblastic differentiation markers. Osteoblast differentiation was detected by alkaline phosphatase (ALP) staining and activity, and alizarin red S and hydroxyapatite staining. Osteoblast-specific markers were analyzed by qRT-PCR, immunoblotting, and immunostaining. To examine the effects of inflammation, we added AS and healthy control serum to Ct and AS BdCs, and then analyzed osteoblast-specific markers. <h3>Results</h3> AS BdCs showed elevated basal intercellular and extracellular ALP activity compared to Ct. When osteoblast differentiation was induced, AS BdCs exhibited higher expression of osteoblast-specific marker genes and faster mineralization than Ct BdCs, indicating that these cells differentiated more rapidly into osteoblasts. ALP activity and mineralization accelerated when serum from AS patients was added to Ct and AS BdCs. <h3>Conclusions</h3> Our results revealed that AS BdCs showed significantly increased osteoblastic activity and differentiation capacity by regulating osteoblast-specific transcription factors and proteins compared to Ct BdCs. Active inflammation caused by adding AS serum accelerated bony ankylosis. Our study could provide useful basic data for understanding the molecular mechanism of ankyloses in AS. <h3>Disclosure of Interest</h3> None declared
THU0657 A tele-health follow-up strategy for tight control of disease activity in rheumatoid arthritis: results of the non-inferiority randomised controlled trail (the tera study)
Authors: A Thurah, K Steengaard-Pedersen, M Axelsen, U Fredberg, LMV Schougaard, NHI Hjøllund, M Pfeiffer-Jensen, TB Laurberg, K Lomborg, T Maribo
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Despite the increased prevalence of rheumatoid arthritis (RA) in recent years, no studies have yet investigated the effect of monitoring disease activity through a standardized tele-health strategy in patients with RA (1). <h3>Objectives</h3> To test the effect of patient-reported outcome (PRO) based tele-health follow-up for tight control of disease activity in patients with RA, and the differences between tele-health follow-up performed by rheumatologists or rheumatology nurses. <h3>Methods</h3> A total of 294 patients were randomized (1:1:1) to either PRO-based tele-health follow-up carried out by a nurse (PRO-TN) or a rheumatologist (PRO-TR), or conventional out-patient follow-up by physicians. The Flare-RA (2) was used as decision aid for assessing disease activity. The primary outcome was change in DAS28 after week 52. Secondary outcomes were: physical function, quality of life and self-efficacy. The non-inferiority margin was a DAS28 change of 0.6. Mean differences were estimated following per-protocol, intention to treat (ITT) and imputation (IMP). <h3>Results</h3> Overall patients had low disease activity at baseline and end follow-up. Demographics and baseline characteristics were similar between groups. Non-inferiority was established for DAS28. In the ITT analysis mean difference in DAS28 between PRO-TR vs. control were -0.10 (90% CI -0.30; 0.13) and -0.19 (-0.41; 0.02) between PRO-TN vs. control. When including one yearly visit to the outpatient clinic, patients in PRO-TN had a total of 1.72 (SD 1.03) visit/year, PRO-TR 1.75 (SD 1.03) vist/year and control 4.15 (SD 1.0) visits/year. This included extra visits due to inflammatory flare. Overall more than 80% of the patients in all three groups answered that they were "very satisfied" with the consultation form they received and no differences were found between the three groups. <h3>Conclusions</h3> Among RA patients with low disease activity or remission a PRO-based tele-health follow-up for tight control of disease activity in RA can achieve similar disease control as conventional outpatient follow-up. The degree of disease control did not differ between patients seen by rheumatologists or rheumatology nurses. <h3>References</h3> References. Ward IM, Schmidt TW, Lappan C, Battafarano DF. How critical is tele-medicine to the rheumatology workforce? Arthritis Care Res (Hoboken). 2016 Feb 11. Berthelot JM, De Bandt M, Morel J, Benatig F, Constantin A, Gaudin P, et al. A tool to identify recent or present rheumatoid arthritis flare from both patient and physician perspectives: The 9FLARE9 instrument. Ann Rheum Dis. 2012 Jul;71(7):1110–6. ClinicalTrails.gov identifier: NCT02155894. <h3>Disclosure of Interest</h3> None declared
FRI0028 In vitro inhibitory effect of etanercept on autophagy: a new mechanism of action of tnf inhibitors in rheumatoid arthritis
Authors: M Vomero, A Capozzi, C Barbati, T Colasanti, V Manganelli, F Ceccarelli, FR Spinelli, F Conti, C Perricone, A Finucci, M Pendolino, R Scrivo, R Misasi, M Sorice, G Valesini, C Alessandri
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Autophagy has emerged as a key mechanism in the development, survival and function of immune cells and dysregulation of autophagic pathway has been implicated in the pathogenesis of several autoimmune diseases including Rheumatoid Arthritis (RA) (1). In fact, autophagy seems to be involved in the generation of citrullinated peptides, with consequent breakage of tolerance in RA (2). Moreover, increased autophagy levels and a reduction of apoptosis-related molecules have been found in RA synovial tissues and a role of TNF-induced autophagy in RA development has been proposed (3). <h3>Objectives</h3> The aim of the study was to analysed the effect of TNF and anti-TNF inhibitor etanercept on autophagy and apoptosis in cells involved in RA pathogenesis. <h3>Methods</h3> Peripheral blood mononuclear cells (PBMCs) and fibroblast-like synoviocytes (FLS) isolated from RA patients were cultured in presence of TNF and in serum deprivation state (starvation) for 4 hours and then etanercept, at concentration of 15 ug/mL, were added to the culture. After 24h cells were analyzed for levels of autophagy marker LC3-II by western blot and for percentage of annexin V-positive apoptotic cells by flow cytometry. <h3>Results</h3> As expected, TNF and starvation induced autophagy on RA PBMC and FLS in dose-dependent manner after 24h of culture (p&lt;0.05 in all experimental conditions). Moreover, the adding of etanercept caused a significant reduction of LC3-II levels (p=0.004) and an increase of apoptosis rate (p=0.002) after both pro-autophagic stimuli (p&lt;0.05). <h3>Conclusions</h3> We demonstrated for the first time an inhibitory effect of etanercept on autophagy activation of cells involved in RA pathogenesis. In addition, our findings suggest a crucial role of autophagy in RA cells survival. <h3>References</h3> Pierdominici M, Vomero M, Barbati C et al. Role of autophagy in immunity and autoimmunity, with a special focus on systemic lupus erythematosus. FASEB J. 2012; 26:1400–12. Sorice M, Iannuccelli C, Manganelli V et al. Autophagy generates citrullinated peptides in human synoviocytes: a possible trigger for anti-citrullinated peptide antibodies. Rheumatology. 2016;55:1374–85. Rockel JS, Kapoor M. Autophagy: controlling cell fate in rheumatic diseases. Nat Rev Rheumatol. 2016;12:517–31. <h3>Disclosure of Interest</h3> None declared
THU0318 Coronary artery disease in patients with behÇet's disease: a retrospective, single center study
Authors: H Chen, Y Zhang, W Chen, J Liu, L Wang, F Zhang, W Zheng
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Behçet9s disease (BD) is a chronic inflammatory disease affecting various size of arteries and veins. Coronary artery disease (CAD), a life-threatening condition, is rarely reported in patients BD. <h3>Objectives</h3> To investigate the clinical characteristics of BD patients complicated with CAD, and to elucidate the potential risk factors of CAD in BD patients. <h3>Methods</h3> We retrospectively reviewed all the medical records of BD patients who were admitted to our institute from 2001 to 2016. CAD was defined as aneurysm, stenosis and (or) occlusion of coronary arteries confirmed by angiography or contrast-enhanced computer tomography. BD patients with CAD and age- and gender-matched BD patients without CAD (at 1:3 ratio) were enrolled. Demographic, clinical and laboratory data were systemically collected, analyzed and compared between two groups. <h3>Results</h3> In total, 19 patients, including 17 male and 2 female, were complicated with CAD. The mean onset age of BD was 34 and the mean duration from the onset of BD to the diagnosis of CAD was 4.1 year. Angina pectoris (8/19) and acute myocardial infarction (8/19) were the most common cardiac symptoms, arrhythmia was presented in one patient, and three patient remained asymptomatic. Coronary artery aneurysm, stenosis and occlusion were presented in 9, 13 and 3 patients, respectively. Smoking (7/19) was frequently observed, while hypertension (3/16), diabetes mellitus (2/19), obesity (1/19) and alcohol consumption (1/19) were rarely present. Additionally, seven arterial and two venous extra-cardiac vasculopathies were presented. Oral ulceration (19/19) and skin lesions (16/19) were the most common BD-associated symptoms. Comparing with BD patients without CAD, patients with BD presented with higher ESR (mean, 34.4 vs 16.3 mm/hr, p=0.0018) and CRP (mean, 36.4 vs 12.2 mg/L, p=0.002), more frequency of skin lesions (84% vs 55%, p=0.0334) and pathergy reactions (37% vs 26%, p=0.0103). Furthermore, multivariate analysis confirmed that elevated CRP was a independent risk factor of CAD (OR 1.032, 95% CI 1.011–1.053, p=0.003). <h3>Conclusions</h3> CAD, a rare complication of BD, predominately affect male patients. BD patients with CAD presented with active BD disease symptoms and elevated inflammatory markers, which implicated aberrant vascular inflammation was the key mechanism of CAD in BD patients. CRP, but not traditional CAD risk factors, was the risk factor of CAD in BD patients. <h3>Disclosure of Interest</h3> None declared
Change in palliative performance scale score as prediction of survival in patients with advanced cancer.
Authors: Yong Joo Lee, Sang-Yeon Suh, Chulmin Kim, Jo Hi Yoon, Thomas William LeBlanc, Sung-Eun Choi, Ah-Ram Seo, Hong-Yup Ahn
Journal: Journal of Clinical Oncology (2014)

9561 Background: The Palliative Performance Scale (PPS) is a widely-used prognostic tool in patients with advanced cancer. While single PPS measures are predictive of survival, the utility of serial PPS measurements warrants further study. We hypothesized that changes in PPS are associated with survival, and thus may be useful in forecasting health services utilization in Korea, where late referral to palliative care services is common. This study examines associations between change in PPS score and survival in patients with advanced cancer. Methods: We identified a cohort of 606 inpatients who died at a Korean university hospital’s hospice/palliative care center, and abstracted relevant chart data. PPS scores were measured twice as part of standard care: (1) on admission, and (2) after three days in the hospital (D3). ‘Change at D3’ was defined as the difference between initial PPS and PPS at D3, divided by initial PPS. We used a Cox regression modeling approach to explore the association between this change score and survival, adjusting for the influence of age, sex and primary cancer type. Results: Patients’ median survival was nine days (range 1-65). Change scores were statistically significantly associated with survival. A change score of >30% yielded a hazard ratio for death of 2.66 (95% CI 2.19-3.22), compared to a change score of ≤ 30%. PPS of ≤ 30 on D3 also independently predicted survival, with a hazard ratio of 1.67 (95% CI 1.38-2.02) compared to PPS of >30. PPS at admission was not independently associated with survival. Conclusions: A change of over 30% in PPS appears to predict survival in patients with advanced cancer at our center, even after adjustment for confounders. PPS at admission did not predict survival. Change in PPS may be a more sensitive indicator of impending death than a single PPS measurement at admission in cancer patients near the end of life. Further prospective study is needed to test this important finding in other populations.