tbuckley/cabot-search huggingface dataset:
THU0404 Self-reported severity of gout in a primary care setting and associated factors – results from a gout survey in primary care
Authors: AJ Landgren, M Dehlin, U Bergsten, V Sigurdardottir, P Drivelegka, T Sandström Zverkova, L Jacobsson
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Patients with gout are usually seen in primary care. There are numerous reports regarding severity of gout in cohort studies and patients seen in more specialized care, less is known about the spectrum of severity of the disease in primary care. <h3>Objectives</h3> To describe the pattern of self-reported disease severity of gout and predictors thereof in a primary care setting. <h3>Methods</h3> All patients above 18 with an ICD10-diagnosis of gout at a health care visit in primary care (Jan 2015 through Aug 2016) were identified from primary care within the Western Sweden Health Care Region (WSHCR). 941 patients were identified and included in the study. They were sent a questionnaire with questions regarding comorbidities, demographics, gout characteristics and Health Assessment questionnaire (HAQ) reflecting disability. Self-reported disease severity was assessed by a three-level Likert scale (mild, moderate, severe). Possibly associated factors were analyzed by bivariate logistic regression (binary outcome: mild vs. moderate/severe) models and factors that were statistically significant were further analyzed by multivariate analysis. <h3>Results</h3> The response rate was 54%. Response rates were significantly lower in women overall and in men under the age of 50. Covariates that were significantly associated with more severe self-reported severity of gout in the bivariate logistic regression models (Table 1) were: female sex, hyperlipidemia, higher number of previous attacks, attack during last month, HAQ. In the multivariate analysis objective measures of gout severity such as more than ten previous attacks and attack during last month were strongly associated with the patients grading of severity, in addition to presence of hyperlipidemia (Table 1). <h3>Conclusions</h3> Over 40% of patients with gout in a primary care setting rated their disease as moderate or severe. The validity of the patients rating was supported by other covariates reflecting disease severity. The observations that women and those with hyperlipidemia reported a more severe disease needs to be further explored. <h3>Disclosure of Interest</h3> None declared
FRI0101 Ra in male carpenters: occupational wood dust exposure increases acpa and rf seropositivity and significantly raises rf titres
Authors: K Bellis, M Whallett, D Murphy, D Hutchinson
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Wood dust has been hypothesised as a trigger in RA. Exposure may activate peptidyl arginine deaminase through exposure to silica and carbon nanoparticles,<sup>1</sup> stimulating RF autoantibody production.<sup>2</sup> Though non-silica dusts have shown increased RA risk in construction workers, wood dust exposed individuals were excluded from analysis in a recent large registry study.<sup>3</sup> <h3>Objectives</h3> To analyse the autoantibody status of male RA wood workers in Cornwall, UK, compared to matched RA controls with no occupational dust or fume exposure. <h3>Methods</h3> All male RA patients were sent an occupational questionnaire, detailing current occupation, last occupation (if retired) and other occupations for &gt;1 year. Telephone follow up was completed to minimise missing data. 41/720 (6%) patients died during the study period (22 months). 39/720 (5%) were excluded due to incomplete data. 147/640 (23%) had exposure to wood dust including other dust co-exposures, with 44/147 (30%) indentifying wood dust as their primary occupational exposure as carpenters, approximately seven times higher than expected given UK employment census data. This cohort was matched to 102 RA controls with no dust or fume exposure for age +/- 5 years, sex and index of multiple deprivation (IMD) +/- 1 decile. RF titres were compared via 2 tailed Mann Whitney U test, and ACPA seropositivity was compared using a Z test of 2 proportions. <h3>Results</h3> No significant differences were seen in median age between woodworker cases (median 59 years IQR 50–63), and controls (median 58 years IQR 48–65). Woodworker never smokers demonstrated significantly higher seropositivity rates for both RF and ACPA than respective controls, and RF titres were significantly higher amongst woodworkers irrespective of smoking (Table 1). Median smoking rates were not significantly different between cohorts: woodworkers median pack years 23.5 (IQR 14.75–36), control median pack years 20.5 (IQR 10.25–32.75). <h3>Conclusions</h3> Wood dust exposed RA patients are more likely to be seropositive. Sequential environmental insults of smoking and wood dust exposure have an additive effect on rheumatoid factor levels, conferring increased disease severity. Further studies are needed to determine if occupational wood dust exposure causes RA. <h3>References</h3> Murphy D, Sinha A, Hutchinson D. Wood Dust: A Trigger for Rheumatoid Arthritis? Am J Med 2015;128:e35. Hubbard R, Lewis S, Richards K, Johnston I, Britton J. Occupational exposure to metal or wood dust and aetiology of cryptogenic fibrosing alveolitis. Lancet 1996;347:284–9. Blanc PD, Jarvholm B, Toren K. Prospective risk of rheumatologic disease associated with occupational exposure in a cohort of male construction workers. Am J Med 2015;128:1094–101. <h3>Acknowledgements</h3> Cornwall Arthritis Trust. <h3>Disclosure of Interest</h3> None declared
AB0993 Elderly - onset sarcoidosis: a single center comparative study
Authors: S Kobak, F Sever, H Semiz, M Orman
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Sarcoidosis is a chronic granulomatous inflamatory disease characterized with non-caseified granuloma formation. It is rarely affects patients older than 65 years old. <h3>Objectives</h3> The purpose of this study is to compare and evaluate the demografic, clinical and laboratory features of elderly-onset (EOS) and young-onset sarcoidosis (YOS) patients. <h3>Methods</h3> One hundred and thirty one patients diagnosed with sarcoidosis according to clinical, radiologic and histopathological evaluation were included in this study.The patients with initial symptoms started after age 65 were accepted as EOS. Demografic, clinic, radiologic, and laboratory data and the medication which the patients recieved were recorded and retrospectively evaluated. <h3>Results</h3> Twenty (15.3%)of 131 patients were diagnosed as EOS, and 111 (84.7%) patients were evaluated as YOS. Fifteen of 20 EOS patients were female and 5 of them were male. Average duration of the disease was determined as 38.4months for YOS and 22.5months for EOS (p=0.556).Delay of the diagnosis was 12months for YOS while it was 3months for EOS (p=0.001).Higher rates of fatique, comorbid diseases and more Hydroxychloroquine (HQ) use were detected in EOS patients comparing to YOS (p=0.010, p=0.003 and p=0.039 respectively).There was obviously more disease modifying anti-rheumatic drugs (DMARDs) use by YOS group but statistical difference wasn9t significant. The 3-year survival rate after diagnosis of sarcoidosis was %95 in the EOS group, compared with %100 in the YOS group. <h3>Conclusions</h3> In this study we showed that YOS and EOS patients may be presented with different clinical, and laboratory features. EOS patients are characterized with higher rates of fatique and comorbid diseases, less inflammatory sign and delayed diagnosis, and less DMARDs usage. <h3>References</h3> Newman LS, Rose CS, Maier LA. Sarcoidosis. N Engl J Med 1997; 336: 1224±1234. Chen ES, Moller DR. Etiology of sarcoidosis. Clin Chest Med. 2008; 29:365–377. Iannuzzi MC, Rybicki BA, Teirstein AS. Sarcoidosis. N Engl J Med. 2007;357:2153–65. Iannuzzi MC, Fontana JR. Sarcoidosis: clinical presentation, immunopathogenesis, and therapeutics. J Am Med Assoc. 2011;305:391–9. Baughman RP, Teirstein AS, Judson MA, Rossman MD, Yeager H Jr, Bresnitz EA, et al. Clinical characteristics of patients in a case control study of sarcoidosis. Am J Respir Crit Care Med.2001;164:1885–9. <h3>Disclosure of Interest</h3> None declared
SP0022 Trpa1 channels in osteoarthritis
Authors: E Moilanen
Journal: Annals of the Rheumatic Diseases (2017)

Osteoarthritis (OA) has long been viewed as a degenerative "wear-and-tear" disease of cartilage. There is, however, increasing evidence to confirm that inflammation has a critical role in the pathogenesis and symptoms of the disease. Inflammation in osteoarthritis is distinct from that typical for rheumatoid arthritis; it is generally low-grade in its nature but characterized by exacerbations with joint effusions and more severe symptoms. Osteoarthritis shares many features of innate immunity but the inflammatory mechanisms eventually leading to anatomical and functional changes and symptoms typical for osteoarthritis are not known in detail; but their further understanding is essential for the development of disease-modifying treatments for osteoarthritis. Transient receptor potential ankyrin 1 (TRPA1) is a ligand-gated membrane-bound cation channel. It has been widely studied in sensory neurons where it acts as a chemosensor for harmful exogenous compounds and mediates pain and neurogenic inflammation. More recently, TRPA1 has been found to be activated also by endogenous compounds formed in inflammation, such as reactive oxygen and nitrogen species. That prompted us to investigate the role of TRPA1 in inflammatory conditions including osteoarthritis. Monosodium iodoacetate (MIA) -induced arthritis is a widely used animal model of osteoarthritis. We found that MIA evoked acute inflammation, degenerative cartilage changes and joint pain in wild type mice; but interestingly, those responses were significantly attenuated in TRPA1 deficient animals. Furthermore, TRPA1 was found to be expressed and inducible by inflammatory factors including IL-1 and IL-17 in primary human OA chondrocytes; and the TRPA1 channel was shown to be functional based on calcium influx assays. Pharmacological inhibition and genetic depletion of TRPA1 downregulated the production of inflammatory factors and MMP enzymes in mouse cartilage and primary human OA chondrocytes. The present results introduce TRPA1 as a plausible factor involved in the pathogenesis of OA and provide a novel target for analgesic and anti-inflammatory drugs with disease modifying potential in OA. <h3>Disclosure of Interest</h3> None declared
SP0003 Novel animal model in arthritis
Authors: Y Iwakura
Journal: Annals of the Rheumatic Diseases (2017)

We have generated two rheumatoid arthritis (RA) models, human T-cell leukemia virus type I (HTLV-I) transgenic mice and IL-1 receptor antagonist (Ra)-deficient (KO) mice, to elucidate the pathogenic mechanisms of the disease. Both models spontaneously developed arthritis that closely resembles RA in humans. We found that TNF-, but not IL-6-, deficiency suppressed development of arthritis in IL-1Ra KO mice, while IL-6 but not TNF was involved in the development of arthritis in HTLV-I transgenic mouse model. IL-17 plays an important role in both models, suggesting the central role of IL-17 in these RA models. We found that the expression of C-type lectin receptor (CLR) genes was augmented in the affected joints of these models using DNA microarrays. Dendritic cell immunoreceptor (DCIR) is one of such CLRs with a carbohydrate recognition domain in their extracellular carboxy terminus and an ITIM in its intracellular amino terminus. Because human syntenic locus for the CLR genes is linked to several autoimmune diseases including RA and SNPs in the <i>Dcir</i> gene is associated with RA, we have generated <i>Dcir</i> KO mice to examine the roles of this gene in the immune system. We found that aged <i>Dcir</i> KO mice spontaneously developed autoimmune enthesitis and ankyloses accompanied by fibrocartilage proliferation and ectopic ossification. DCs were excessively expanded in <i>Dcir</i> KO mice, causing these mice autoimmunity and also highly susceptible to induced-autoimmune diseases. <i>Dcir</i> KO mouse–derived bone marrow cells differentiated into DCs more efficiently than did wild-type BMCs upon treatment with GM-CSF, due to enhanced STAT-5 phosphorylation. Furthermore, we found that IFN-g producing T cells were increased in <i>Dcir</i> KO mice and IFN-g enhanced bone and cartilage formation, resulting in the increase of bone volume and aberrant ossification in joints. DCIR is also expressed in osteoclasts and suppresses osteoclastogenesis upon activation. These findings suggest that DCIR plays important roles in both immune system and bone metabolism. <h3>Disclosure of Interest</h3> None declared
Practical implications of single-gene versus NGS testing in advanced NSCLC.
Authors: Tiffany Yu, Alison Tradonsky, Andrew Layton
Journal: Journal of Clinical Oncology (2017)

e23106 Background: Genetic testing to guide 1 st -line treatment is recommended for advanced non-small cell lung cancer (aNSCLC), but is complicated by small biopsy specimens available to test increasing numbers of biomarkers. This study compared commercially-available genetic tests for aNSCLC and the investigational use Oncomine™ Dx Target Test next generation sequencing (NGS) assay. Methods: This retrospective analysis used data from a large commercial lab, which offered clinical single-gene tests (EGFR therascreen, ALK Vysis, BRAF cobas, laboratory developed tests [LDT] for ROS1, BRAF, KRAS, MET, RET, and FGFR1); and NGS LDT (Illumina NextSeq 500). The lab also conducted investigational use of Oncomine Dx Target Test assay (Ion Torrent PGM Dx) on archival tissue. Clinical test orders received September 2015 – October 2016 were included. Sample rejection, test initiation, success rates, slide consumption, testing time, and turnaround time (TAT) were assessed. Results: Clinically, 3,857 single-gene and 219 NGS LDT tests were ordered on 1,479 samples for 1,436 patients. A total of 169 Oncomine Dx Target Tests were conducted. Conclusions: Investigational use of Oncomine Dx Target Test at this laboratory showed higher rates of test initiation and successful completion while using less tissue compared to either single-gene testing for ≥4 biomarkers or NGS LDT. This early experience suggests Oncomine Dx Target Test may enable therapy selection with multiple biomarker testing on small tissue samples for more aNSCLC patients compared to current methods. [Table: see text]
Factors associated with early outcomes following standardised therapy in children with ulcerative colitis (PROTECT): a multicentre inception cohort study
Authors: Jeffrey S Hyams, Sonia Davis, David R Mack, Brendan Boyle, Anne M Griffiths, Neal S LeLeiko, Cary G Sauer, David J Keljo, James Markowitz, Susan S Baker, Joel Rosh, Robert N Baldassano, Ashish Patel, Marian Pfefferkorn, Anthony Otley, Melvin Heyman, Joshua Noe, Maria Oliva-Hemker, Paul Rufo, Jennifer Strople, David Ziring, Stephen L Guthery, Boris Sudel, Keith Benkov, Prateek Wali, Dedrick Moulton, Jonathan Evans, Michael D Kappelman, Alison Marquis, Francisco A Sylvester, Margaret H Collins, Suresh Venkateswaran, Marla Dubinsky, Vin Tangpricha, Krista L Spada, Ashley Britt, Bradley Saul, Nathan Gotman, Jessie Wang, Jose Serrano, Subra Kugathasan, Thomas Walters, Lee A Denson
Journal: The Lancet. Gastroenterology & hepatology (2017)
Genetically Encoded Photoactuators and Photosensors for Characterization and Manipulation of Pluripotent Stem Cells
Authors: Jordan E. Pomeroy, Hung X. Nguyen, Brenton D. Hoffman, Nenad Bursac
Journal: Theranostics (2017)

Our knowledge of pluripotent stem cell biology has advanced considerably in the past four decades, but it has yet to deliver on the great promise of regenerative medicine.The slow progress can be mainly attributed to our incomplete understanding of the complex biologic processes regulating the dynamic developmental pathways from pluripotency to fully-differentiated states of functional somatic cells.Much of the difficulty arises from our lack of specific tools to query, or manipulate, the molecular scale circuitry on both single-cell and organismal levels.Fortunately, the last two decades of progress in the field of optogenetics have produced a variety of genetically encoded, light-mediated tools that enable visualization and control of the spatiotemporal regulation of cellular function.The merging of optogenetics and pluripotent stem cell biology could thus be an important step toward realization of the clinical potential of pluripotent stem cells.In this review, we have surveyed available genetically encoded photoactuators and photosensors, a rapidly expanding toolbox, with particular attention to those with utility for studying pluripotent stem cells.
THU0156 Clinical assessment versus ultrasonography in patients with rheumatoid arthritis treated with biological agents - the impact of concomitant fibromyalgia
Authors: MM Tamas, L-J Ghib, CI Bondor, I Felea, L Damian, I Filipescu, A Mociran, S-P Simon, L Muntean, S Rednic
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Concomitant fibromyalgia (FM) may increase subjective components of the disease activity scores (DAS) in rheumatoid arthritis (RA), thus leading to an improper assessment of treatment response. Ultrasonography (US) is currently used in clinical practice as an objective measure of the disease activity. The US7 German score was demonstrated to be sensitive to change, reflecting the therapeutic response in RA patients [1]. <h3>Objectives</h3> To evaluate clinical and US parameters in RA patients with or without concomitant FM, undergoing biological therapy. <h3>Methods</h3> RA patients treated with various biological agents who presented in our Department of Rheumatology were consecutively enrolled. Patients underwent clinical and laboratory examinations. US was performed by an experienced sonographer, blinded to clinical evaluation. Synovitis and synovial/tenosynovial vascularity were scored semiquantitatively (grade 0–3) by gray-scale (GS) and power Doppler (PD) US. Tenosynovitis (TS) and erosions were scored for presence [1]. Patients were divided in two groups according to the difference between tender joint count (TJC) and swollen joint count (SJC): ≥7 RA-FM group, &lt;7 RA-nonFM group, representing the "joint count" criteria for FM, after the study of Pollard <i>et al</i>. [2]. <h3>Results</h3> Thirty-nine patients were included, 77% women, mean age 55.2±11.3 years, mean disease duration 15.25±9.4 years. Nine out of 39 (23%) patients were classified as having associated FM. Disease duration and treatment were comparable between groups. Significantly higher values for TJC, patient global assessment (PGA), DAS 28 were found in the RA-FM group, with no differences for SJC or inflammatory markers (ESR, CRP). GS and PD-US7 scores were similar between groups (Table 1). In the RA non-FM, but not in the RA-FM group, GS and PD-US7 correlated with SJC (r=0.44, <i>p</i>=0.015 – GS synovitis, r=0.47, <i>p</i>=0.008 – PD synovitis; r=0.57, <i>p</i>=0.001 – GS TS; r=0.46, <i>p</i>=0.011 – PD TS) and PD synovitis negatively correlated with the "joint count" criteria (r=-0.44, <i>p</i>=0.015). <h3>Conclusions</h3> Concomitant FM in RA patients undergoing biological therapy lead to higher DAS28 scores, but not to synovial inflammation on US. US-PD correlates with clinically detected synovitis in the non-FM group. US is expected to modify treatment decision and to prevent RA mistreatment especially in RA-FM patients. <h3>References</h3> Backhaus M, et al. Evaluation of a novel 7-joint ultrasound score in daily rheumatologic practice: a pilot project. Arthritis Rheum. 2009;61(9):1194–201. Pollard LC, et al. Fibromyalgic rheumatoid arthritis and disease assessment. Rheumatology (Oxford). 2010;49(5):924–928. <h3>Disclosure of Interest</h3> None declared
AB0942 Effect of corticosteroid infiltrations on diabetes. a monocentric retrospective study
Authors: S Mathieu, M Couderc, Z Tatar, J Lopez, S Malochet-Guinamand, J-J Dubost, A Tournadre, M Soubrier
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Corticosteroid therapy can unbalance diabetes, particularly when administered orally, but also during articular infiltration. Corticosteroid infiltrations are an integral part of the therapeutic arsenal in rheumatology. They are utilized to treat congestive articular flare-ups of osteoarthritis or inflammatory rheumatic diseases. Periarticular or ductal pathologies, such as trochanteric bursitis, rotator cuff pathology and carpal-tunnel syndrome, may require the use of these infiltrations. Caution is often required when using corticosteroid infiltrations in diabetics. <h3>Objectives</h3> The purpose of our study was to evaluate whether or not diabetic patients undergoing a corticosteroid infiltration during hospitalization had a diabetes imbalance. <h3>Methods</h3> Diabetic patients having undergone a corticosteroid infiltration during hospitalization between 2009 and 2015 were sought. We collected data regarding their rheumatological pathology, glycated hemoglobin (HbA1c), and fasting glycemia on the day of the infiltration, the next day and after 48 hours. <h3>Results</h3> A total of 114 patients were included in our study. The average age was 72.1±9.4 years. All of them had Type 2 diabetes, and 35 of them were treated with insulin. Average HbA1c was 7.3±0.1%. Overall, 47 (41.2%) patients had an HbA1c below 7%. A total of 31 (27.2%) patients had a diabetes imbalance after infiltration, and 19 of these, who were taking oral antidiabetics, required 48 hours of rapid insulin to balance their glycemia. Overall, 12 patients increased their insulin dose. Out of the 47 patients with good HbA1c, 7 (14.9%) of them had a glycemia imbalance, versus 24 (35.8%) who were unbalanced out of the 67 patients whose HbA1c exceeded 7% (p=0.013). <h3>Conclusions</h3> Corticosteroid infiltrations can lead to a diabetes imbalance, thus making it necessary to administer a few days of rapid insulin or to increase the insulin dose. A patient whose HbA1c is below 7% has a low risk of unbalancing his/her diabetes after corticosteroid infiltration. <h3>Disclosure of Interest</h3> None declared