tbuckley/cabot-search huggingface dataset:
THU0172 Improvement of disease activity in a 5-year cohort of rheumatoid arthritis patients treated under treat to target recommendations and a multispeciality care model receiving conventional dmard therapy
Authors: P Santos-Moreno, D Gomez, E Castillo, R Giraldo, G Ballesteros, L Villarreal, J Bello, D Buitrago-Garcia
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Treat to Target (T2T) strategy becomes from the need to develop therapeutic targets and tools to achieve defined outcomes in rheumatoid arthritis (RA), this strategy has become recognized as a standard of good practice embodying the principle that rapid attainment of remission, or low disease activity, can halt joint damage and maintain good quality of life. <h3>Objectives</h3> The aim of this study was to describe global change in Disease Activity Score 28 (DAS28) using T2T strategy for a 5 year period in patients with conventional DMARD therapy in a large cohort of patients from a Colombian specialized in RA center with multidisciplinary care model (MCM). <h3>Methods</h3> A descriptive dynamic cohort study was performed. Records of patients using conventional DMARD treatment from specialized in RA center were reviewed; those patients were followed-up under T2T standards. Clinical follow-up was according to DAS28 as follows: every 3–5 weeks (DAS28 &gt;5.1), every 7–9 weeks (DAS28 ≥3.1 and ≤5.1), and every 11–13 weeks (DAS28 &lt;3.1). Therapy had to be adjusted with DAS28 &gt;3.2 unless patient9s conditions don9t permit it. MCM model means that every patient is seen by the other specialties involved in care as a minimum three times a year. We divided patients in three groups: low disease activity (LDA), moderate disease activity (MDA) and severe disease activity (SDA) patients. Descriptive epidemiology was done, percentages and averages were calculated; the median of each variable was analyzed using t-Student assuming normality for DAS28 distribution and the level activity disease was analyzed using Pearson9s statistics. <h3>Results</h3> We included 1443 patients, 84% were women and 16% were men. Mean age was 62±11 years; mean DAS28 at beginning was 4.0±1; regarding disease activity 57% were in moderate disease activity and 17% in severe disease activity. While at 5 year follow up mean DAS was 2.92±0.65, 48% achieved remission, 30% low disease activity, with decrease to 20% in moderate disease activity and 2% in severe disease activity. <h3>Conclusions</h3> There is a significant improvement of DAS28 in a cohort of RA patients receiving only conventional DMARDs therapy, treated and followed under T2T strategy recommendations and a MCM model. <h3>Disclosure of Interest</h3> None declared
SP0001 Relevance of animal models in osteoarthritis
Authors: T Pap
Journal: Annals of the Rheumatic Diseases (2017)

Osteoarthritis (OA) is the most frequent joint disease and a leading cause of disability in the Western world. Currently, we do not have a cure for this degenerative disorder and despite a high individual and socioeconomic demand, available therapeutic strategies have not changed substantially within the last 40 to 50 years, largely involving basic symptomatic control using analgesics and NSAIDS, physiotherapy and behavioural changes, and eventual prosthetic replacement in end-stage disease. While prosthetic joint replacement constitutes an effective surgical treatment option for patients whose joints are irreversibly damaged by OA, demographic development together with altered physical activities in our aging society increasingly demonstrate the limitations of joint replacement surgery as the only real treatment modality. There is, therefore, an urgent requirement for disease modifying drugs that aim to halt OA disease progression during the early stages and potentially to kick start cartilage regeneration. This need is contrasted, however, by a sustained "translational roadblock" in OA research with very few conceptually novel therapeutic approaches on the horizon. Amongst others, this "translational roadblock" results from a general lack in our understanding of how articular chondrocytes as the only cells in joint cartilage acquire and maintain their specific and highly specialised phenotype and how this phenotype changes during OA onset and progression. Investigation of this developmental aspect of disease pathology in OA patients and using human samples has many limitations, which is why animal models remain to constitute a key element of cartilage and OA research. This lecture summarizes the relevance of different animal models for understanding fundamental principles of cartilage homeostasis and remodelling in health and osteoarthritic cartilage degeneration. By focusing on the analysis of chrondrocyte phenotypic stability, it provides examples for how the use of such models can contribute to understanding OA and to the development of new therapeutic strategies for the disease. <h3>Disclosure of Interest</h3> None declared
Effect of Comorbidity on Prostate Cancer–Specific Mortality: A Prospective Observational Study
Authors: Prabhakar Rajan, Prasanna Sooriakumaran, Tommy Nyberg, Olof Akre, Stefan Carlsson, Lars Egevad, Gunnar Steineck, N. Peter Wiklund
Journal: Journal of Clinical Oncology (2017)

Purpose To determine the effect of comorbidity on prostate cancer (PCa)–specific mortality across treatment types. Patients and Methods These are the results of a population-based observational study in Sweden from 1998 to 2012 of 118,543 men who were diagnosed with PCa with a median follow-up of 8.3 years (interquartile range, 5.2 to 11.5 years) until death from PCa or other causes. Patients were categorized by patient characteristics (marital status, educational level) and tumor characteristics (serum prostate-specific antigen, tumor grade and clinical stage) and by treatment type (radical prostatectomy, radical radiotherapy, androgen deprivation therapy, and watchful waiting). Data were stratified by Charlson comorbidity index (0, 1, 2, or ≥ 3). Mortality from PCa and other causes and after stabilized inverse probability weighting adjustments for clinical patient and tumor characteristics and treatment type was determined. Kaplan-Meier estimates and Cox proportional hazards regression models were used to calculate hazard ratios. Results In the complete unadjusted data set, we observed an effect of increased comorbidity on PCa-specific and other-cause mortality. After adjustments for patient and tumor characteristics, the effect of comorbidity on PCa-specific mortality was lost but maintained for other-cause mortality. After additional adjustment for treatment type, we again failed to observe an effect for comorbidity on PCa-specific mortality, although it was maintained for other-cause mortality. Conclusion This large observational study suggests that comorbidity affects other cause–mortality but not PCa-specific– mortality after accounting for patient and tumor characteristics and treatment type. Regardless of radical treatment type (radical prostatectomy or radical radiotherapy), increasing comorbidity does not seem to significantly affect the risk of dying from PCa. Consequently, differences in oncologic outcomes that were observed in population-based comparative effectiveness studies of PCa treatments may not be a result of the varying distribution of comorbidity among treatment groups.
FRI0301 Characterization of fever in hospitalized patients with systemic lupus erythematosus: lessons from the jiangsu cohort
Authors: X Feng, W Pan, L Liu, M Wu, L Sun
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Fever is one of the main symptoms leading to the admission of patients with systemic lupus erythematosus (SLE) and its causes are usually complicated. <h3>Objectives</h3> To explore the prevalence and clinical characteristics of fever in Chinese SLE patients at the time of their first admission and to find out whether fever is related to a poor prognosis. <h3>Methods</h3> A follow-up study aimed to delineate SLE prognosis had been conducted by our Lupus Collaborative Group under the supervisor of Jiangsu Rheumatology Association to collect the data of patients who had ever recorded first admissions during the 1999–2009 decade (1). Among which, those with admission temperature documented were extracted for the assessment of potential factors associated with fever. The independency of various clinical features linked to fever was established by binary logistic regression analysis, and the relation between fever and patient9s survival was determined by Cox regression analysis. <h3>Results</h3> Totally 1,348 patients were enrolled, in which 1,049 (77.8%) had normal temperature, 221 (16.4%) had low and moderate fever and 78 (5.8%) had high fever at the time of their first hospitalization. Compared with those having normal temperature, fever patients were more likely to have short disease duration (RR 0.74), concurrent infection (RR 3.29) and gastrointestinal (RR 1.57) as well as hematological involvements (RR 1.56). High C reactive protein level (RR 2.08) and positive anti-Sm antibody (RR1.55) were the two laboratory factors related to fever at admission. However, age, gender, SLEDAI score or erythrocyte sedimentation rate was not independently associated with fever in this cohort. Cox regression analysis showed that there was no correlation between fever and overall deaths (Figure 1) as well as infection induced deaths. <h3>Conclusions</h3> Both infection and lupus itself (especially gastrointestinal and hematological involvements) contribute to fever in SLE patients. Although the presence of fever increases the complexity of disease treatment, it does not constitute a risk factor for patient9s long-term outcome. <h3>References</h3> Feng X, Pan W, Liu L, et al. Prognosis for hospitalized patients with systemic lupus erythematosus in China: 5-year update of the Jiangsu cohort. PLoS One. 2016;11(12):e0168619. <h3>Acknowledgements</h3> This study was supported by National Natural Science Foundation of China (81373198) and Jiangsu Provincial Special Program of Medical Science (BE2015602). <h3>Disclosure of Interest</h3> None declared
AB1056 Radiographic analysis of metatarsus primus elevatus in patients with rheumatoid forefoot deformities
Authors: S Mizuki, D Hiraoka, K Kushimoto, H Yamasaki, K Yoshida, K Oryoji, K Kamada, E Yokota
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Metatarsus primus elevatus involves dorsal elevation of the first metatarsal relative to the lesser metatarsals. The role of metatarsus primus elevatus in rheumatoid forefoot deformity is yet to be elucidated. We hypothesize that metatarsus primus elevatus can be attributed to a different pathomechanism than typical rheumatoid forefoot deformities such as hallux valgus, splay foot, and flat foot. <h3>Objectives</h3> To clarify the radiographic characteristics of metatarsus primus elevatus in patients with rheumatoid forefoot deformities. <h3>Methods</h3> We retrospectively reviewed standing anteroposterior and lateral radiographs of 51 feet (37 patients; mean age 65.7±7.1 years) before toeplasty due to metatarsalgia at our hospital. The elevation of the first metatarsal relative to the second metatarsal (MPE), the hallux valgus angle (HVA), the intermetatarsal angle (IMA), talar pitch, and calcaneal pitch were measured. For statistical analyses, the Mann-Whitney U test was used. <h3>Results</h3> Median MPE was 1.7 mm (interquartile range: 0.7–4.5 mm). We compared the group with MPE &gt;5 mm (N=12 feet) to the group with MPE ≤5 mm (N=39 feet). The group with higher MPE was significantly younger (p=0.011). There was no significant difference in HVA between the two groups (p=0.068), although IMA was significantly smaller in the group with higher MPE (p=0.033). In the group with higher MPE, calcaneal pitch was greater (p&lt;0.001) and talar pitch was smaller (p=0.016). <h3>Conclusions</h3> In patients with metatarsus primus elevatus, other rheumatoid forefoot deformities such as spray foot and flat foot were not observed. There was a wide range of hallux valgus severity. Metatarsus primus elevatus may be attributed to greater hindfoot calcaneal pitch. <h3>Disclosure of Interest</h3> None declared
AB0938 An atypical case of sarcoidosis revealed by a bilateral prepatellar bursitis
Authors: J Perrier-Cornet, R Ouichka, S Moawad, I Chary-Valckenaere
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Prepatellar bursitis is not very frequent in daily practice and the main causes are infections, crystal arthropathies or trauma. We report the case of a 49-year-old man presented to our department with bilateral anterior knee pain. Pain started 3 months ago without any triggering factor. He denied any trauma or infection. The patient also denied any history of gout, rheumatoid arthritis or systemic lupus. <h3>Objectives</h3> On clinical exam, bilateral knee swellings were noticed consistent with prepatellar bursitis with no wound or abrasion, no fever, signs of arthritis or lymphadenopathy. <h3>Methods</h3> Knee ultrasonography and skeletal scintigraphy confirmed symmetrical prepatellar bursitis. Laboratory findings showed elevated ESR and CRP but no other abnormalities. Few days later, the patient presented with subcutaneous painful nodules that appeared on his forearms. Biopsy was done and showed deep subcutaneous sarcoid nodules of Darier-Roussy, confirming the diagnosis of sarcoidosis. Further work up revealed typical sarcoid pulmonary involvement. Bilateral hilar and mediastinal lymphadenopathy with beaded appearance of interlobular septa were noticed on CT-scan of the chest. The Positron Emission Tomography showed abnormally high <sup>18</sup>F-fluorodeoxy glucose uptake in the thoracic lymph nodes. <h3>Results</h3> All the diagnostic work up confirmed the diagnosis of systemic sarcoidosis. The decision was to start oral corticosteroids. Few days after starting the systemic steroids, the skin lesions and the knees pain improved significantly. <h3>Conclusions</h3> The conclusion is that after excluding the main causes of bursitis (infection, trauma and inflammatory arthritis) (1), it9s necessary to keep in mind sarcoidosis as possible diagnosis. This clinical observation is important because involvement of the bursa is a rare musculoskeletal manifestation of sarcoidosis (2). Moreover, it9s very uncommon to diagnose sarcoidosis presenting with just bilateral prepatellar bursitis with no other musculoskeletal or rheumatological symptoms (3). The association of bursitis, inflammatory skin lesions and thoracic lymphadenopathy is uncommon but may suggest the diagnostic of sarcoidosis. <h3>References</h3> Mathieu S, Prati C, Bossert M, Toussirot E, Valnet M, Wendling D. Acute prepatellar and olecranon bursitis. Retrospective observational study in 46 patients. Joint Bone Spine. 2011;7:423–4. Fujimoto H, Shimofusa R, Shimoyama K, Nagashima R, Eguchi M. Sarcoidosis presenting as prepatellar bursitis. Skeletal Radiol. 2006;35:58–60. Ruangchaijatuporn T, Chang EY, Chung CB. Solitary subcutaneous sarcoidosis with massive chronic prepatellar bursal involvement. Skeletal Radiol. 2016;45:1741–5. <h3>Disclosure of Interest</h3> None declared
AB0098 Effects of tofacitinib in early arthritis bone loss
Authors: B Vidal, R Cascão, M Finnilä, I Lopes, S Saarakkala, P Zioupos, H Canhão, J Fonseca
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Rheumatoid arthritis (RA) causes immune mediated local and systemic bone damage. <h3>Objectives</h3> The main goal of this work was to analyze, how treatment intervention with tofacitinib prevents the early disturbances on bone structure and mechanics in adjuvant induced arthritis rat model. This is the first study to access the impact of tofacitinib on the systemic bone effects of inflammation. <h3>Methods</h3> Fifty Wistar adjuvant-induced arthritis (AIA) rats were randomly housed in experimental groups, as follows: non-arthritic healthy group (N=20), arthritic non-treated (N=20) and 10 animals under tofacitinib treatment. Rats were monitored during 22 days after disease induction for the inflammatory score, ankle perimeter and body weight. Healthy non-arthritic rats were used as controls for comparison. After 22 days of disease progression rats were sacrificed and bone samples were collected for histology, micro-CT, 3-point bending and nanoindentation analysis. Blood samples were also collected for bone turnover markers and systemic cytokine quantification. <h3>Results</h3> At tissue level, measured by nanoindentation, tofacitinib increased bone cortical and trabecular hardness. However, micro-CT and 3-point bending tests revealed that tofacitinib did not revert the effects of arthritis on cortical and trabecular bone structure and on mechanical properties. <h3>Conclusions</h3> Possible reasons for these observations might be related with the mechanism of action of tofacitinib, which leads to direct interactions with bone metabolism, and/or with kinetics of its bone effects that might need longer exposure. <h3>Disclosure of Interest</h3> None declared
Different Genomic Changes Underlie Adaptive Evolution in Populations of Contrasting History
Authors: Sofia G Seabra, Inês Fragata, Marta A Antunes, Gonçalo S Faria, Marta A Santos, Vitor C Sousa, Pedro Simões, Margarida Matos
Journal: Molecular Biology and Evolution (2017)

Experimental evolution is a powerful tool to understand the adaptive potential of populations under environmental change. Here, we study the importance of the historical genetic background in the outcome of evolution at the genome-wide level. Using the natural clinal variation of Drosophila subobscura, we sampled populations from two contrasting latitudes (Adraga, Portugal and Groningen, Netherlands) and introduced them in a new common environment in the laboratory. We characterized the genome-wide temporal changes underlying the evolutionary dynamics of these populations, which had previously shown fast convergence at the phenotypic level, but not at chromosomal inversion frequencies. We found that initially differentiated populations did not converge either at genome-wide level or at candidate SNPs with signs of selection. In contrast, populations from Portugal showed convergence to the control population that derived from the same geographical origin and had been long-established in the laboratory. Candidate SNPs showed a variety of different allele frequency change patterns across generations, indicative of an underlying polygenic basis. We did not detect strong linkage around candidate SNPs, but rather a small but long-ranging effect. In conclusion, we found that history played a major role in genomic variation and evolution, with initially differentiated populations reaching the same adaptive outcome through different genetic routes.
THU0482 Evolution of comorbid fibromyalgia frequency in axial spondyloarthritis patients starting an anti-tnf agent, and correlation to anti-tnf efficacy. the predict-spa study
Authors: S Perrot, A Moltό, A Etcheto, N Boudersa, P Claudepierre, N Roux, F Berenbaum, A Martin, L Sparsa, P Coquerelle, M Soubrier, L Gossec, M Dougados
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Fibromyalgia (FM) is a frequent comorbid condition in axial spondyloarthritis (axSpA). It is not known how FM comorbidity may respond to the management of SpA, and especially to anti-TNF agents. <h3>Objectives</h3> To evaluate the change of comorbid FM status of axSpA patients starting an anti-TNF treatment. <h3>Methods</h3> A prospective multicenter national study involving 39 rheumatology centers in France, analyzing 519 patients with axSpA requiring anti-TNF therapy (ClinicalTrials.gov: NCT03039088). Patients were screened for FM with the FiRST questionnaire before and after 3 months of anti-TNF. Kappa coefficient was calculated to determine the agreement of the FiRST at M0 and M3. Response to anti-TNF (BASDAI50 response was compared according to positive screening for FM or not, at both time-points using chi2 tests. <h3>Results</h3> Of the 519 enrolled pts, 504 (with complete data on the FiRST questionnaire) were analyzed at M3. A positive screening for comorbid FM was found in 192 pts (38%) at M0 and in 127 (25%) pts at M3. Correlation between FiRST at M0 and M3 was weak with a Kappa coefficient correlation of 0.4 [0,3 - 0,5]. Four groups were identified: group [+/+] with comorbid FM at M0 and M3: N=93 (18%; group [+/-] with comorbid FM at M0 but not at M3: N=99 (20%); group [-/-] without comorbid FM at M0 and M3: N=278 (55%); group [-/+] without comorbid FM at M0 but at M3: N=34 (7%) Changes in the status of comorbid FM (disappearance or appearance) was observed in 134 pts (26%). In the 193 pts with baseline comorbid FM, after 3 months of anti-TNF treatment, comorbid FM was no longer found in 99 (51%)%.Efficacy at M3 was significantly better, according to BASDAI 50, in patients without comorbid FM at M3 (Table). <h3>Conclusions</h3> There is a high frequency of comorbid FM screened by the FiRST in active axSpA, decreased by 51%f after 3 months of anti-TNF treatments. Persistence of FM after 3 months of anti-TNF treatment is associated with lower anti-TNF response. Further studies are required to analyze the impact of screening FM before starting anti-TNF therapy in axSpA. <h3>References</h3> Perrot S, et al. Development and validation of the Fibromyalgia Rapid Screening Tool (FiRST). Pain. 2010;150:250–6. <h3>Acknowledgements</h3> This study was conducted thanks to an unrestricted grant from MSD. <h3>Disclosure of Interest</h3> None declared