tbuckley/cabot-search huggingface dataset:
THU0462 The Predictors of Fracture in Patients with Coeliac Disease: An Observational Study: Table 1
Authors: R. Sinha, M. Bukhari
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Background</h3> Coeliac disease and other malabsorptive diseases have been associated with a low bone mineral density secondary to a variety of factors including calcium absorption. We have previously shown that there is a fivefold propensity for having Osteoporosis (OP) compared to controls with a predilection for spinal osteoporosis (1). However this does not translate completely to predicting fragility fractures. The FRAX™ tool uses the femoral neck to predict fractures on a population basis and ignores the lumbar spine. <h3>Objectives</h3> We set out to determine the predictors of fragility fractures in a large observational cohort. Specifically we set out to determine if the lumbar spine bone mineral density (BMD) is a predictor for fragility fractures. <h3>Methods</h3> Patients referred for bone mineral density (BMD) estimation in a scanner in the North west of England between 2004 and 2014 with a history of coeliac disease were identified from a dual X-ray absorptiometry (DEXA) database. Demographics and other risk factors were also recorded. Initially those that sustained a fracture were compared ot those that had not sustained a fracture using the chi squared test for categorical variables and Students T test for continuous variables. Fragility fractures were also recorded. Initially univariate logistic regression models were modelled predicting fractures in the cohort and a multivariate model was subsequently fitted. Variables included age at scan, gender, body mass index (BMI), family history of fracture, alcohol, smoking, glucocorticoid exposure, rheumatoid arthritis in addition to BMD in the lumbar spine (L1-L4) and the femoral neck. <h3>Results</h3> 788 patients were scanned in the referral period. Mean age at scan was 55.4 year (SD 14.4), 576 (73.1%) were female, 159 (20.2%) had sustained a fracture. Patients who had sustained a fracture were more likely to be female 127/576 (22%) vs 32/212 (15%) (p=0.03), older 59.2 years (SD14) vs 54 years (SD 14) (p&lt;0.001) and have concomitant rheumatoid arthritis 5/159 (3%) vs 6/629 (1%) (p=0.04). They also had lower BMD in both the lumbar spine and the femoral neck. Results of the univariate analysis are shown in table 1. Significant predictors are denoted with an asterisk (*). In the multivariate model, the only variables that predicted fractures in this cohort were the BMD in the lumbar spine (OR 0.09 95%CI 0.03,0.25) and age at scan OR 1.19 (95%CI 1.04,1.37) per decade. <h3>Conclusions</h3> In univariate analysis, many risk factors are associated with fracture in this cohort, but in multivariate analysis, the best predictor of fracture was the BMD in the lumbar spine. This is not included in the FRAX™ tool and would make estimating the fracture risk in this cohort difficult. Further modelling in other cohorts is needed to validate this finding. <h3>References</h3> Oldroyd et al. Ann Rheum Dis 2011;70(Suppl3):225. <h3>Disclosure of Interest</h3> None declared
Biweekly Gemcitabine-Oxaliplatin and Dexamethasone for Relapsed/Refractory Malignant Lymphoma
Authors: Hawk Kim, Je-Hwan Lee, Young Don Joo, Sung Hwa Bae, Jung-Hee Lee, Dae-Young Kim, Won-Sik Lee, Hun-Mo Ryoo, Jung Lim Lee, Jae Hoo Park, Kyoo Hyung Lee
Journal: Blood (2011)
Establishment of a Waldenstrom’s Macroglobulinemia Cell Line (BCWM.1) with Productive In Vivo Engraftment in SCID-hu Mice.
Authors: Daniel Ditzel Santos, Allen W. Ho, Olivier Tournilhac, Xavier Leleu, Evdoxia Hatjiharrisi, Lian Xu, Pierfrancesco Tassone, Paola Neri, Zachary Hunter, Mariana A.Z. Chemaly, Andrew Branagan, Robert Manning, Christopher Patterson, Sophia Adamia, Jitra Kriangkum, Jeffery L. Kutok, Linda Pilarski, Kenneth C. Anderson, Nikhil Munshi, Steven P. Treon
Journal: Blood (2005)
Diverse Impact of Notch-1, Jagged-1 and Dll-1 Expression On Response to Treatment and Relapse Free Survival in Acute Myeloid Leukemia.
Authors: Magdalena Czemerska, Agnieszka Pluta, Anna Szmigielska-Kaplon, Ewa Wawrzyniak, Barbara Cebula-Obrzut, Aleksandra Medra, Piotr Smolewski, Tadeusz Robak, Agnieszka Wierzbowska
Journal: Blood (2012)
Mutations In the DNA Methyltransferase Gene DNMT3A Are Highly Recurrent In Patients with Intermediate Risk Acute Myeloid Leukemia, and Predict Poor Outcomes
Authors: Timothy J Ley, Li Ding, Matthew J. Walter, Michael D. McLellan, Tamara Lamprecht, David E. Larson, Cyriac Kandoth, Jacqueline E. Payton, Jack Baty, John S. Welch, Christopher C. Harris, Cheryl F. Lichti, R. Reid Townsend, Robert S. Fulton, David J. Dooling, Daniel C. Koboldt, Heather Schmidt, Qunyuan Zhang, John R. Osborne, Ling Lin, Michelle O'Laughlin, Joshua F. McMichael, Kim D. Delehaunty, Sean D. McGrath, Lucinda A. Fulton, Vincent J. Magrini, Tammi L. Vickery, Jasreet Hundal, Lisa L. Cook, Joshua J. Conyers, Gary W. Swift, Jerry P. Reed, Patricia A. Alldredge, Todd Wylie, Jason Walker, Joelle Kalicki-Veizer, Mark A. Watson, Sharon Heath, William D. Shannon, Nobish Varghese, Rakesh Nagarajan, Peter Westervelt, Michael H. Tomasson, Daniel C. Link, Timothy A. Graubert, John F. DiPersio, Elaine R. Mardis, Richard K. Wilson
Journal: Blood (2010)
2015 ACC Health Policy Statement on Cardiovascular Team-Based Care and the Role of Advanced Practice Providers
Authors: John E. Brush, Eileen M. Handberg, Cathleen Biga, Kim K. Birtcher, Alfred A. Bove, Paul N. Casale, Michael G. Clark, Arthur Garson, Jerome L. Hines, Jane A. Linderbaum, George P. Rodgers, Robert A. Shor, Vinod H. Thourani, Janet F. Wyman
Journal: Journal of the American College of Cardiology (2015)
PWE-006 The Effects of Smoking on Thiopurine Metabolism: Abstract PWE-006 Table 1
Authors: BD Warner, E Johnston, S Fong, C Amadi, P Blaker, M Arenas-Hernandez, A Marinaki, J Sanderson
Journal: Gut (2016)

<h3>Introduction</h3> There is an unpredictable relationship between thiopurine methyl transferase (TPMT) and hypermethylation. It is likely that cytochrome P450 (CYP450) enzymes play a role in the demethylation of methylated mercaptopurine (MMP), altering the MMP:Thioguanine nucleotide (TGN) ratio(Table 1). Smoking has been shown to induce CYP450 enzymes. One study on smoking and olanzapine demonstrated a 6 fold increase in CYP450 activity through smoking.<sup>1</sup> This might suggest that smoking could upregulate the demethylation process, reducing MMP. <h3>Methods</h3> Patients on thiopurines had their smoking status recorded as they attended the inflammatory bowel disease (IBD) clinic. Retrospective data on demographics was collected (Table 1). Only measurable TGNs after 6 weeks of therapy were used for analysis. Metabolites measured whilst on allopurinol were excluded. Average TGNs over the treatment period, MMP and MMP:TGN ratios were compared between smokers and non-smokers. Hypermethylators were defined as any patient with an MMP:TGN ratio of ≥11 during their treatment <h3>Results</h3> 230 patients were analysed(117 males). Table 1 shows comparison in demographics between smokers and non-smokers Mean MMP for smokers was 1683(SD 2565, median 840) versus 2041 in non-smokers(SD 2401, median 1340)(P = 0.713). Mean MeMP:TGN ratio for smokers was 6.15 (SD 9.06, median 2.22) versus 7.81 in non-smokers (SD 8.01, median 4.70)(P = 0.593). <h3>Conclusion</h3> There were more hypermethylators in the non-smoking cohort than in the smoking cohort (42.7% versus 28.3%(P &lt; 0.05)), however the difference between average MMP and MMP:TGN ratios were not significant although the median differences are compelling. There were significant differences between quantity smoked and the MMP:TGN ratio. Paradoxically, the reduction in methylation if smoking &lt;5 cigarettes/day was reversed when smoking ≥15 cigarettes/day. This may suggest an alternative pathway affected by smoking. Smoking status and quantity should be taken into account when monitoring metabolites. Additionally, polymorphisms for CYP450 (CYP1A2*F and CYP1A2*1 C), known to affect drug metabolism between individuals, may be responsible for variation and require further research. <h3>Reference</h3> 1 Carrillo JA, Herráiz AG, Ramos SI, Gervasini G, Vizcaíno S, Benítez J. Role of the smoking-induced cytochrome P450 (CYP)1A2 and polymorphic CYP2D6 in steady-state concentration of olanzapine. <i>J Clin Psychopharmacol</i>. 2003 Apr;<b>23</b>(2):119–27. <h3>Disclosure of Interest</h3> None Declared
Patients with "Single-Hit" but Not MYC -Amplified Non-Burkitt High-Grade B Cell Non-Hodgkin Lymphomas Experience Poor Survival Outcomes and May Benefit from Intensive Induction Therapy
Authors: Daniel J. Landsburg, Marissa K. Falkiewicz, Jennifer J.D. Morrissette, April M. Schrank-Hacker, Sunita Dwivedy Nasta, Jakub Svoboda, Stephen J. Schuster, Anthony R. Mato, Benjamin A. Chu, Yanming Zhang, Amir Behdad, Adam M. Petrich
Journal: Blood (2015)
Recurrent pleural effusions and cardiac tamponade as possible manifestations of pseudoprogression associated with nivolumab therapy– a report of two cases
Authors: Bhaskar C. Kolla, Manish R. Patel
Journal: Journal for ImmunoTherapy of Cancer (2016)

<h3>Background</h3> Checkpoint inhibitors are a class of agents that employ host's adaptive immune defenses in fighting cancer. With many new indications and several ongoing clinical trials in a variety of malignancies, the usage of these agents is set to increase significantly. One of the key challenges patients and physicians face while using these drugs is with the appropriate assessment of response to therapy. <h3>Case presentation</h3> We are reporting two patients with lung cancer who were treated with nivolumab and experienced rapidly accumulating recurrent pleural effusions requiring multiple thoracenteses (6 and 4 times each for patient 1 and 2 respectively) with in the first few weeks of initiation of therapy and also developed pericardial effusion with cardiac tamponade requiring pericardiocentesis. Both patients had prior history of malignant spread to pleural and pericardial space in their disease course. Therapy was continued in the first patient with spontaneous resolution of effusions after 8&nbsp;weeks and the disease showed near complete response to treatment on imaging at 16&nbsp;weeks. Second patient declined to continue further treatment with nivolumab after 3&nbsp;cycles due to recurrent effusions and cardiac tamponade, although there was some evidence of clinical response at discontinuation. <h3>Conclusions</h3> Patients with history of malignant involvement of visceral spaces should be monitored closely for rapidly accumulating effusions and particularly for cardiac tamponade, after initiation of therapy with nivolumab. This presentation could represent pseudoprogression, and continuation of therapy with close monitoring is prudent as long as effusions are manageable and there is no definitive evidence of progression elsewhere.
SAT0015 Novel and Rare Mutations Linked To Polyautoimmunity
Authors: A. Johar, J.C. Sarmiento-Monroy, A. Rojas-Villarraga, M.F. Silva-Lara, H.R. Patel, R.D. Mantilla, C. Mastronardi, M. Arcos-Burgos, J.-M. Anaya
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Background</h3> Polyautoimmunity (i.e., the presence of two or more autoimmune diseases in a single patient) and familial autoimmunity (i.e., diverse autoimmune diseases in a nuclear family) represent extreme phenotypes ideal for identifying major genomic variants contributing to autoimmunity (1–3). Whole Exome Sequencing (WES) and linkage analysis are well suited for this purpose due to its strong resolution upon familial segregation patterns of functional protein coding and splice variants (3). <h3>Objectives</h3> The primary objective of this study was to identify potentially autoimmune causative variants using WES data from extreme pedigrees segregating polyautoimmunity phenotypes. <h3>Methods</h3> DNA of 47 individuals across 10 extended and multigenerational pedigrees, ascertained from probands affected with polyautoimmunity and familial autoimmunity, were selected for WES. Variant calls were obtained through Genome Alignment Tool Kit (GATK) algorithm; filters for prioritizing major functional were applied and later implemented for genetic linkage analysis. Sanger sequencing corroborated variants with significant linkage. <h3>Results</h3> Novel and mostly rare variants harbored in <i>SRA1, MLL4, ABCB8, DHX34</i> and <i>PLAUR</i> genes showed significant linkage (LOD scores are &gt;3.30). The strongest signal was in <i>SRA1</i>, with a LOD score of 5.48. Network analyses indicated that <i>SRA1</i> and <i>PLAUR</i> both contribute to regulation of apoptotic processes. <h3>Conclusions</h3> Novel and rare variants in genetic linkage with polyautoimmunity were identified throughout WES. Genes harboring these variants might be major players of autoimmunity. <h3>References</h3> Expert Rev Clin Immunol. 2007;3:623–35. BMC Med. 2013;11:73. Autoimmun Rev. 2015;14:204–9. <h3>Acknowledgement</h3> Supported by Colciencias (Bogota, Colombia) <h3>Disclosure of Interest</h3> None declared
THU0633 The Revised Bristol RA Fatigue Nrs, Containing New Nrs-Coping Anchors (Braf-NRS V2 Revised): Validity across 6 European Countries: Table 1
Authors: S. Hewlett, J. Nicklin, C. Bode, F. Cramp, L. Carmona, B. Davis, E. Dures, M. Engelbrecht, J. Fransen, L. Gossec, R. Greenwood, S. Hagel, M. van de Laar, I. Petersson, M. Redondo, A. Molto, G. Schett, J. Kirwan
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Background</h3> BRAF-NRS are a trio of items for fatigue severity, impact and coping. At development, patients wanted the NRS-Severity &amp; Impact anchors to read 0=No fatigue/effect, 10=Totally exhausted/Great deal of effect, but the NRS-Coping to read 0=Not at all well, 10=Very well.<sup>1</sup> Construct and criterion validity of the NRS-Coping-NRS are less strong than NRS-Severity and Impact;<sup>2</sup> cognitive interviewing shows patient confusion over Coping anchors.<sup>3</sup> <h3>Objectives</h3> Test construct and criterion validity of BRAF-NRS V2, which has Revised NRS-Coping anchors of 0=Very well, 10=Not at all well (NRS-Severity and Impact unchanged), in 6 EU countries. <h3>Methods</h3> RA patients from France, Germany, Netherlands, Spain, Sweden and UK completed the BRAF-NRS V2 Revised, BRAF-NRS Original, BRAF-MDQ, RAID, SF-36. Spearman9s correlations assessed criterion and construct validity. <h3>Results</h3> Of 1276 patients 76% were female, median HAQ 1.0 (IQR 0.375–1.5). Mean BRAF-NRS-Coping Revised 4.0 (SD 2.66) vs Original 5.95 (SD 2.57), NRS-Severity 4.86 (SD 2.56), NRS-Impact 4.61 (SD 2.69). BRAF-NRS-Severity and Impact had appropriate validity with all 18 variables, overall and by country (r=0.46–0.96). Table shows BRAF-NRS-Coping Revised had better validity than NRS-Coping Original in all variables overall (stronger correlations bolded), and for 15–18/18 variables in all countrie except Spain (3/18). The difference in strength of correlations between the versions was large for the total sample, but minimal for Spain. <h3>Conclusions</h3> BRAF-NRS V2 Revised has construct and criterion validity across 6 EU countries. Whilst the BRAF-NRS-Coping Original is acceptable, the BRAF-NRS-Coping Revised has greater validity. In Spain, the validity of both versions is lower but similar to each other. Further exploration of the concept and wording of "coping" in the Spanish population is warranted. <h3>References</h3> Nicklin et al 2010a; Nicklin et al 2010b; Hewlett et al 2016 in press <h3>Acknowledgement</h3> EULAR project grant EP1009 <h3>Disclosure of Interest</h3> None declared
PWE-083 Behavioural Gastro-Oesophageal Reflux Disease Caused by Supragastric Belching
Authors: JJ Neville, R Fernandes, J Jafari, T Wong, G Sui
Journal: Gut (2016)

<h3>Introduction</h3> Supragastric belching (SGB) is considered to be a behavioural phenomenon, thus gastro-oesophageal reflux disease (GORD) caused by SGB can be considered as behavioural GORD. Behavioural GORD may necessitate differential treatment to ‘classical’ GORD and therefore requires diagnosis as a distinct clinical entity. This study aims to establish the prevalence of GOR events caused by SGB and evaluate the associated demographic features, symptoms and oesophageal motility abnormalities. <h3>Methods</h3> The Oesophageal Physiology Laboratory, Guy’s Hospital, patient database was retrospectively searched for patients diagnosed with GORD in whom SGB was observed. Patient demographic information, symptoms and oesophageal motility abnormalities were collected. The 24 hour pH-impedance studies were analysed for SGB. GORD events closely following SGB (within 6 seconds) were quantified and the acid exposure time and acid/non-acid reflux events occurring after a SGB were calculated when upright and recumbent. <h3>Results</h3> Forty-six patients with a diagnosis of GORD and SGB were identified (48% female, mean age 50.5 years (range: 29–75), male mean age 52.5 years (29–79)). Ninety-five percent of patients reported heartburn and/or epigastric pain, 81.8% suffered from excessive belching, 63.6% reported regurgitation and 54.5% reported dysphagia. Forty-three percent of patients had a hypotensive lower oesophageal sphincter (LOS). SGB preceded 22.7% of all reflux events (24.9% upright and 6.6% recumbent) and 26.5% of acid reflux events. On average, over 24 hours, 16.3 reflux events were associated with SGB (13.0 acid and 4.1 non-acid) corresponding to a mean acid exposure time of 17.8 minutes. In this cohort SGB accounted for 17% of acid exposure time (22% upright and 7.4% recumbent). SGB had no effect on the total number of reflux events or the total acid exposure time in 3 patients and in 3 further patients SGB had no effect on the total acid exposure time. SGB caused ≥50% of the total number of reflux events in 3 patients and ≥50% of the total acid exposure time in 5 patients. Patients with a hypotensive LOS did not have a significantly higher total number of reflux events (p = 0.88) or total acid exposure time (p = 0.86). No relationships were seen between the presence of a hiatus hernia and the total number of reflux events (p = 0.43) or acid exposure time (p = 0.16) associated with SGB. <h3>Conclusion</h3> SGB induced a considerable proportion of reflux events and acid exposure time. In 8 patients SGB caused ≥50% of the total reflux events or overall acid exposure time, and hence these patients may be considered as having behavioural GORD. Behavioural GORD should be diagnosed and treated separately to ‘classical’ GORD. Further work is required to elucidate the cause and pathophysiology of SGB. <h3>Disclosure of Interest</h3> None Declared
PTH-018 Endoclot Prophylaxis Following Complex Endoscopic Resection of Gastrointestinal Neoplasia: No Need to Bleed!: Abstract PTH-018 Table 1
Authors: F Chedgy, K Kandiah, S Subramaniam, S Thayalasekaran, F Thursby-Pelham, G Longcroft-Wheaton, P Bhandari
Journal: Gut (2016)

<h3>Introduction</h3> EMR / ESD of large lesions creates large mucosal defects and is associated with significant post-procedural bleeding. Endoclot<sup>TM</sup> is a topical hemostatic powder that rapidly absorbs water creating a high concentration of platelets, red blood cells and clotting factors – accelerating the natural coagulation cascade. Routine application of Endoclot<sup>TM</sup> to ESD or EMR defects is hypothesised to reduce the risk of significant post EMR/ESD bleeding. <h3>Methods</h3> A prospective registry was set up to record all EMR / ESD procedures since 2006. Prophylactic use of Endoclot<sup>TM</sup>, following endoscopic resection of lesions &gt;20 mm, to prevent delayed bleeding was introduced in June 2014. The bleeding rate since the introduction of this strategy was compared with the bleed rate of our historic cohort since 2006. Bleeding was defined as significant if it required: readmission, transfusion or further intervention. SPSS was used for statistical analysis of data. <h3>Results</h3> Pre-Endoclot cohort: 496 patients underwent lower gastrointestinal EMR/ESD at our institution between 2006 and 2013 with a mean polyp size of 43 mm and 12% of these polyps were scarred due to previous intervention. Significant delayed bleeding was seen in 21/496 patients (4%). 264 patients underwent upper gastrointestinal EMR/ESD at our institution between 2006 and 2013. Significant delayed bleeding was seen in 9/264 patients (3%). Endoclot cohort: 71 patients have undergone colonic EMR/ESD (mean polyp size 46 mm, 38% scarred) (Table 1). 61 patients have undergone upper gastrointestinal resection (mean lesion size 33 mm, 37% scarred). There was 1 significant delayed bleed in the colonic group (1%) requiring further endoscopic therapy. There were 2 bleeds (3%) in the upper GI group, which were managed with further endoscopic therapy without the need for blood transfusion. There have been no complications related to Endoclot<sup>TM</sup> use. Device clogging was experienced in 5% of upper gastrointestinal cases and 15% of lower gastrointestinal cases. <h3>Conclusion</h3> Endoclot<sup>TM</sup> shows promise in reducing the risks of delayed bleeding following endoscopic resection of large neoplastic lesions from the gastrointestinal tract. Our data demonstrates a 75% reduction in risk of delayed bleeding following EMR/ESD for large colonic polyps in a group with a significantly higher rate of scarring and therefore bleeding risk. A randomised controlled trial is required to clarify the role of routine use of Endoclot<sup>TM</sup> following EMR/ESD. <h3>Disclosure of Interest</h3> None Declared
Protein Phosphatase 2B Inhibitor, Cyclosporine A, Stimulates Endothelial Cell Exocytosis of Ultra-Large VWF Multimeric Strings by Regulating Munc18c Phosphorylation.
Authors: Lettica Nolasco, Francisca C. Gushiken, Vimal Patel, Nancy Turner, Joel Moake, K. Vinod Vijayan
Journal: Blood (2007)
A Bioinformatic Approach to CLL IGHV Sequence Analysis Identifies Extensive Ig Sequence Archetypes among BothMutated and Unmutated Sequences.
Authors: Bradley T. Messmer, Benjamin J. Raphael, Sarah J. Aerni, George F. Widhopf, Laura Z. Rassenti, Traci L. Toy, Thomas J. Kipps
Journal: Blood (2005)