tbuckley/cabot-search huggingface dataset:
AB1128 Helicobacter pylori in systemic lupus erythematosus its association with endoscopic and histopathologic findings
Authors: I Arroyo Prado, JA Velarde Ruiz Velasco, CE Gomez Lopez, S Ureña Gutierrez, G Martinez Bonilla, V Gonzalez Diaz, JI Espejo Pascencia, S Cerpa Cruz
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Helicobacter pylori (Hp) is a Gram-negative bacteria and the cause of most of the chronic gastric infections and its prevalence is above 50% worldwide. This infection is a well-known risk factor to gastric MALT lymphoma but also could be the trigger of several autoimmune diseases such as immune thrombocytopenic purpura and systemic lupus erythematosus <h3>Objectives</h3> To determine the frequency of H pylori in systemic <i>lupus erythematosus patients</i> (SLE). <h3>Methods</h3> A cross-sectional study was done in patients who fulfilled the 2012 SLICC criteria for SLE and were willing to sign the informed consent to be subjected to endoscopic procedure. The tissue sample was analyzed by pathologist. We used mean and standard deviation to describe the data, to compare both groups Student t test was done and for continuous variables we used chi-square; the correlation analysis was performed with <h3>Results</h3> Twenty two SLE patients were included and we chose a control group from database of endoscopic clinic with diagnosis of functional dyspepsia. Mean age of study group was 31 vs 48 year-old, 95% were women, 32% with immunosuppressant and 95% were taking <i>antimarials</i>. The frequency of Hp in SLE patients was 60%, dsDNA and anti-Ro autoantibodies were associated with the presence of Hp; the study group had more frequency of nodular gastritis, metaplasia and dysplasia. Seventy per cent of patients had less than 5 years of diagnosis. <h3>Conclusions</h3> We found a high frequency of H pylori infection in patients with SLE. Metaplastic and dysplastic changes were also more prevalent in the SLE group. Our data suggest that Hp infection took place in early stages of disease. <h3>References</h3> Daniel S Smyk, Andreas L Koutsoumpas, Maria G Mytilinaiou, Eirini I Rigopoulou, Lazaros I Sakkas, Dimitrios P Bogdanos. Helicobacter pylori and autoimmune disease: Cause or bystander. World J Gastroenterol 2014 January. Sarfaraz Ahmed Hasni Role of helicobacter pylori infection in autoimmune diseases. Curr Opin Rheumatol. 2012 July; 24(4): 429–434. <h3>Acknowledgements</h3> no clinficts of interest. <h3>Disclosure of Interest</h3> None declared
SAT0022 Epigenome-wide association study of rheumatoid arthritis identifies differentially methylated loci in b cells
Authors: A Julià, D Absher, M Lόpez-Lasanta, N Palau, A Pluma, L Waite Jones, JR Glossop, WE Farrell, RM Myers, S Marsal
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Epigenetic regulation of immune cell types could be critical for the development and maintenance of autoimmune diseases like Rheumatoid Arthritis (RA). B cells are highly relevant in RA, since patients express autoantibodies and depleting this cell type is a successful therapeutic approach. Epigenetic variation, such as DNA methylation, may mediate the pathogenic activity of B cells. <h3>Objectives</h3> In this study, we performed an epigenome-wide association study (EWAS) for RA with three different replication cohorts, to identify disease-specific alterations in DNA methylation in B cells. <h3>Methods</h3> Genomic methylation in isolated B lymphocytes was assayed on the Illumina HumanMethylation450 BeadChip, assaying &gt;450,000 different CpG sites. Differential methylated positions (DMPs) were identified in a discovery cohort using a single-point analysis using logistic regression, as well as a pathway-level analysis using a newly developed permutation-based method. A discovery cohort of 50 RA patients and 75 healthy controls from Spain was used to identify the most differentially methylated regions after multiple test correction. Using an independent sample of 15 patients and 15 controls from the same population we performed a replication analysis of the most significant CpG sites and pathways. Using an additional case-control sample of 24 individuals from the UK we provided further evidence of association of the DMPs with RA. Finally, in silico datta from a cohort of systemic lupus erythematosus patients (SLE, n=47) and controls (n=56) from the US, we tested the association of the associated DMPs. <h3>Results</h3> A total of 64 CpG sites were found to be differentially methylated in RA patients compared to controls in the discovery stage after multiple test correction (<i>q</i>&lt;0.05). Six biological pathways were also differentially methylated in RA B cells. Analysis of these epigenetic changes in the independent Spain cohort replicated the association of 10 CpG sites located on 8 genes and 2 intergenic regions. Differential methylation at the <i>CBL</i> signaling pathway was also replicated. Using the UK case-control cohort, association between RA risk and methylation levels at <i>CD1C</i> (<i>P</i>=2.26x10<sup>-9</sup>) and <i>TNFSF10</i> (<i>P</i>=1.67x10<sup>-8</sup>) loci was further validated. Most of the replicated DMPs associated with RA were also found to be associated with differential methylation in SLE B cells. <h3>Conclusions</h3> Our results highlight genes that may drive the pathogenic activity of B cells in RA and suggest shared methylation patterns with SLE. <h3>Disclosure of Interest</h3> None declared
AB0280 Influence of HLA class II antigen (DRB1 and DQB1) on the production of anti-cyclic citrullinated peptide antibodies in a tunisian population
Authors: S Boussaid, S Kochbati
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Rheumatoid arthritis (RA) is the most common chronic inflammatory rheumatism. It9s a complex autoimmune disorder. The aim of this study is to focus on the relationship between HLA-DRB1 genes and RA specific antibodies against cyclic citrullinated peptides (anti-CCP antibodies). <h3>Methods</h3> This prospective study was performed on a total of 81 Tunisian patients with rheumatoid arthritis. All patients fulfilled the American College of Rheumatology (ACR 1987) criteria for RA. For each patient we assessed DNA and serum samples. The DNA was extracted from lymphocytes using a commercial kit (Quiagen). The HLA class II (DQB1 and DRB1) was performed by Polymerase Chain Reaction technique Specifying-sequence primers (PCR-SSP). The specific products of PCR were analyzed by 2.5% agarose gel electrophoresis. All tests include positive and negative controls appropriate for each blood sample. The phenotypes of patients were obtained through the Software One Lambda DNA/SOFTWARE (SSP2L-generic DRB/DQB). <h3>Results</h3> The mean age of our population was 49.17±11.21 years (age 24–78). The disease average duration was 7.44±2.12 years (4 months - 29 years), 82.71% of RA were women and 17.29% were men. Seropositive RA were 80.24%, and 71% of RA have anti CCP positive antibody. Univariate analysis of the presence of anti-CCP antibodies in conjunction with HLA DRB1 and DQB1 was performed. Carriership of HLA DR*0301, 0401 and 1501 were significantly associated with the presence of anti-CCP antibodies (p&lt;0.0001). Four DRB1 0401 carriers were homozygotes with three out of them having anti-CCP antibodies. Carriership of HLA DQB1*0201, 0301, 0302,0501 and 0601 was associated with the presence of anti-CCP antibodies and so was HLA-DQB1*0401, but with a less significant association. <h3>Conclusions</h3> Although no formal conclusions on causality can be drawn from this association study, these findings suggest that anti-CCP antibodies are associated with different phenotypes; which suggest that various pathogenetic mechanisms underlie the positivity for anti-CCP in RA. <h3>Disclosure of Interest</h3> None declared
Quality of life of young mothers with breast cancer in Germany.
Authors: Dorothea Fischer, Berit Wedel, Kristin Baumann, Telja Pursche, Achim Rody, Annika Waldmann
Journal: Journal of Clinical Oncology (2014)

9574 Background: Aim of the study is to analyze the health-related quality of life (QoL) in young breast cancer patients and to compare it to that of an age-heterogeneous breast cancer cohort and of an age-adjusted general population sample. Further, predictors for a reduced QoL should be identified. Methods: A retrospective study analyzed quality of life of 517 young mothers (at least 1 child <12 years) first diagnosed between 2006 and 2011 with primary breast cancer. The patients participated in a resident mother-child program. The standardized questionnaire focused on medical, clinical and social data and especially on QoL (EORTC QLQ-C30, -BR23). The data were compared with those of an age-heterogeneous cohort with breast cancer and an age-adjusted general population sample from the state of Schleswig-Holstein, Germany. Results: The median age of the young cohort was 39 years. Inability to work, being unemployed and a higher body mass index were predictors for a reduced global QoL /health status. Unanticipated treatment and clinical issues did not affect quality of life. Young breast cancer patients – as compared to the older breast cancer cohort – showed a reduced social, emotional and cognitive functioning. In contrast, physical and sexual functions were significantly higher and stress by hair loss was significant better tolerated by the younger patients. Compared to the general population the patients showed a seriously reduced QoL. Conclusions: Because of their high risk of reduced QoL, young breast cancer patients with children under the age of 12 should be carefully observed with a focus on emotional and social functions and their ability to work. Our results imply the need to develop interventional procedures to enhance QoL in the vulnerable group of young breast cancer patients.
SAT0394 The impairment of hip joints in patients with early axial spondyloarthritis (corsar cohort) based on the results of the two-year observation
Authors: D Rumiantceva, T Dubinina, O Rumyantseva, A Demina, E Agafonova, S Erdes, S Krasnenko, A Smirnov
Journal: Annals of the Rheumatic Diseases (2017)

SAT0392 -Table 1.The existing grading criteria of SIJ CTmNY criteria Lee criteria Innsbruck criteria 0 = Normal 1 = Suspicious for erosions or sclerosis 2 = Mildly abnormal with definite erosions or sclerosis, but without alteration in the joint width 3 = Moderately abnormal with erosions or sclerosis, joint space narrowing or widening and/or partial ankylosis 4 = Complete ankylosis 0 = Normal 1 = Focal erosions seen on only one of either semi-coronal or axial images 2 = ≤25% erosions*, but without alteration in the joint width 3 = ≥25% erosions*, joint space alteration and/or partial ankylosis 4 = Complete ankylosis IA = SIJ>4 mm IB = SIJ<2 mm IIA = Contour irregularities IIB = Erosion IIIA = Subchondral sclerosis IIIB = Spur formation IVA = Transarticular bony bridges IVB = Ankylosis *Extent of erosions; (%) = number of slices with erosions/total number of slices × 100.Conclusions: Lee criteria has a better diagnostic specificity with a lower difficulty in the evaluation process, while Innsbruck criteria is a more detailed grading system, which has a higher consistency with the progression of sacroiliitis in AS.
SAT0517 Factors related to analgesic use in patients with knee and/or hip osteoarthritis referred to an outpatient center: results from the amsterdam osteoarthritis cohort
Authors: J Knoop, J van Tunen, M van der Esch, LD Roorda, J Dekker, M van der Leeden, WF Lems
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Analgesics are recommended in current guidelines, but non-use and inadequate prescription have been reported in patients with knee and/or hip osteoarthritis (OA). Furthermore, predictors of analgesic use have not yet been clarified. <h3>Objectives</h3> To (i) describe the use of analgesics; and (ii) determine factors that are related to analgesic use in patients with knee and/or hip OA referred to an outpatient center. <h3>Methods</h3> Data from 656 patients with knee and/or hip OA referred to an outpatient center (Amsterdam Osteoarthritis (AMS-OA) cohort) were used. Self-reported use of analgesic (yes/no) was administered and subdivided into acetaminophen, non-steroidal anti-inflammatory drugs (NSAIDs, including coxibs) and opioids. Logistic regression analyses were performed to analyze the association between analgesic use and disease-related, predisposing, and enabling factors. <h3>Results</h3> Analgesic use was reported by 62% of the patients, with acetaminophen, NSAIDs and opioid use reported by 50%, 30% and 12%, respectively. Factors related to analgesic use were higher pain severity, longer duration of symptoms, higher radiographic hip OA severity, overweight/obesity, and psychological distress. These factors explained 21% of the variance of analgesic use. <h3>Conclusions</h3> Less than two-third of patients with knee and/or hip OA referred to an outpatient center reported analgesic use, which seems to be indicative for under-use. Although multiple, mostly disease-related factors were associated with analgesic use, it remained predominantly unexplained. Our findings may indicate that prescription of analgesics should be guided more dominantly by clinical symptoms and needs, and preceded by a thorough shared decision making process between patient and physician. <h3>Disclosure of Interest</h3> None declared
THU0317 Cardiovascular risk factors and comorbid diseases in takayasu arteritis
Authors: H Masyan, NS Esatoglu, AM Celik, V Hamuryudan, H Yazıcı, E Seyahi
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Objectives</h3> Cardiovascular complications are the main causes of morbidity and mortality in the course of Takayasu arteritis (TA).In addition to the occlusive vasculitis,hypertension and accelerated atherosclerosis are possibly other factors playing role in the ethiopathogenesis of these complications.Although,strict management of traditional cardiovascular risk factors is advocated to diminish the effect of cardiovascular complications,we still do not know whether traditional risk factors and other comorbid conditions are increased or operative.In this study we looked at the frequency of traditional atherosclerotic risk factors and comorbid conditions among patients with TA and suitable diseased and healthy controls. <h3>Methods</h3> We studied 88 (77F,11M) consecutive TA patients and 71 (66F,5M) SLE patients,between May and November 2016.In addition,age and gender matched, 96 (80F, 16M) healthy controls were included.Study participants were interviewed with the help of a standardized questionnaire that assess the presence or absence of traditional atherosclerotic risk factors and several comorbid conditions according to the Charlson comorbidity index.Additionally,Framingham coronary heart disease risk score was calculated. <h3>Results</h3> Smoking was more frequent among the healthy controls,whereas hypertension and family history of cardiovascular diseases were more common among TA patients.Patients with SLE were found to have less hyperlipidemia.The Framingham risk scores did not differ among the groups.Pericardial/pleural and renal diseases were more frequently observed in SLE patients,whereas cardiovascular diseases and chronic lung diseases were more common in TA patients.Inflammatory bowel diseases were only observed in TA patients. <h3>Conclusions</h3> Traditional atherosclerotic risk factors are not increased in TA.Comorbidities in these patients are mainly due to the complications of vascular involvement.The frequency of inflammatory bowel diseases and inflammatory upper/lower back pain is substantially high and deserves further research. Moreover, the increased incidence of cardiovascular and rheumatologic diseases among the first-degree relatives of TA patients suggest that genetic mechanisms may play role in TA <h3>Disclosure of Interest</h3> None declared
AB0492 Nucleic acids oxidative stress status in sjÖgren's syndrome
Authors: D Tecer, R Tural, A Sepici Dincel, F Gogus
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Although there are many defence systems that protect cellular macromolecules against oxidation, oxidative DNA and RNA damage still occurs. Oxidative damage to nucleic acids has been found to be associated with etiopathogenesis and disease activity of inflammatory disorders. Oxidised guanine species have been recognized as a biomarker of oxidative DNA and RNA damage by endogenously generated oxygen radicals. Sjögren9s syndrome (SS) is an autoimmune disorder and associated with overexpression of proinflammatory cytokines. Related to excess expression of proinflammatory cytokines, a prooxidant state could be postulated in SS. <h3>Objectives</h3> We aimed to evaluate levels of nucleic acids oxidative stress products in patients with SS. <h3>Methods</h3> 11 patients with SS diagnosed according to 2012 American College of Rheumatology (ACR) Classification Criteria for Sjögren9s Syndrome, 19 patients with psoriatic arthritis (PsA), diagnosed according to Classification Criteria for Psoriatic Arthritis (PSARC), 9 patients with rheumatoid arthritis (RA), diagnosed according to 2010 Rheumatoid Arthritis Classification Criteria, and 12 healthy controls were included. All SS patients were on hydroxychloroquine sulphate 400mg/day. All PsA and RA patients were on methotrexate 15–20mg/week and folic acid 5 mg/week. The serum samples were collected from participants and stored at -30 C until assayed. Three oxidised guanine species, 8-hydroxy-29-deoxyguanosine as a DNA oxidation marker, 8-hydroxyguanosine as a RNA oxidation marker, and 8-hydroxyguanine as a DNA and RNA oxidation marker, were measured using DNA/RNA Oxidative Damage ELISA Kit (Cayman Chemicals, USA). <i>Statistics:</i> All data are presented as mean and standard deviation (SD). Differences between groups were examined using Kruskal- Wallis tests. The Mann-Whitney U test was performed to test the significance of pairwise differences using Bonferroni correction to adjust for multiple comparisons. A p-value less than 0.05 were considered as statistically significant. Statistical analysis of correlation was performed by using the Spearman rank test. <h3>Results</h3> There was no statistically significant difference between the groups in terms of age and gender. The average level of serum oxidised guanine species in the PsA, RA, SS and healthy control groups were 2871.77±336.20, 2672.20±292.04, 3375.57±344.21, 2777.55±237.05 pg/mL respectively. Oxidised guanine species levels were significantly higher in patients with SS and positively correlated with CRP levels (p:0.011, r: 0.726) (table 2). <h3>Conclusions</h3> A marked increase in DNA damage leading to oxidative stress may contribute to tissue damage in SS. <h3>Disclosure of Interest</h3> None declared
SP0015 New onset raynaud's phenomenon – could this be early limited cutaneous systemic sclerosis?
Authors: M Hughes
Journal: Annals of the Rheumatic Diseases (2017)

A case shall be presented of a patient with Raynaud9s phenomenon and whether this could be early limited cutaenous systemic sclerosis. The presentation shall describe the clinical features and investigative approaches that helped us reach a diagnosis, with a particular focus on the role for microvascular imaging and the detection of SSc-associated autoantibodies. <h3>Disclosure of Interest</h3> None declared
SAT0458 Identification of genetic variation specifically associated with psoriatic arthritis using genome-wide association studies
Authors: JD Cañete, A Aterido, JA Pinto, J Gratacόs, R Queirό, C Montilla, JC Torre-Alonso, JJ Pérez-Venegas, A Fernández-Nebro, S Muñoz-Fernández, C González, D Roig, P Zarco, A Erra, J Rodríguez, S Castañeda, E Rubio, G Salvador, C Díaz-Torné, R Blanco, A Willisch-Domínguez, JA Mosquera, P Vela, J Tornero, S Sánchez-Fernández, H Corominas, J Ramírez, A Pluma, M Lόpez-Corbeto, M Lόpez-Lasanta, R Tortosa, N Palau, S Marsal, A Julià
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> PsA has a higher heritability than PsV, indicating the existence of additional PsA-specific genetic factors. To date, however, the specific genetic basis underlying PsA is poorly understood. <h3>Objectives</h3> The objective the present study was to identify new genetic variation specifically associated with PsA risk. <h3>Methods</h3> In order to characterize the genetic basis of PsA, we performed a GWAS meta-analysis at the single-marker level as well as at the pathway level (GWPA). A cohort of 835 PsA patients and 1,558 controls from the Spanish population was genotyped for &gt;550,000 SNPs. GWAS data from a second cohort of 1,430 PsA patients and 1,417 controls from the North American population was also used. In order to confirm the specificity of the new genetic variation associated with PsA risk, we analyzed the association with purely cutaneous psoriasis (PsC, n=614) and rheumatoid arthritis (RA, n=1,191). We performed a pharmacogenetic analysis to investigate the new PsA-specific pathways as a source for drug discovery in PsA. <h3>Results</h3> GWAS meta-analysis identified a new association between <i>B3GNT2</i> gene and PsA (<i>P</i>&lt;5e-08). In the GWAS pathway analysis, we identified and validated a total of 14 genetic pathways associated with PsA risk. From these, the glycosaminoglycan (GAG) metabolism pathway was also found to be significantly associated with PsA risk when directly contrasted to the PsC cohort as well as the RA cohort. At the functional level, we detected a significant differential expression of GAG metabolism pathway genes in blood samples from PsA patients compared to PsC patients. The pharmacogenetic analysis identified several FDA-approved drugs likely to modify the GAG pathway. <h3>Conclusions</h3> The present study represents an important step towards the characterization of the genetic factors specific to PsA risk. <h3>Disclosure of Interest</h3> None declared