tbuckley/cabot-search huggingface dataset:
AB0727 Hip osteoporosis and vertebral fractures are associated with younger age at diagnosis of spondyloarthritis: results from the comospa study
Authors: MH Derakhshan, NJ Goodson, J Packham, R Sengupta, H Marzo-Ortega, A Molto, S Siebert
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Spondyloarthritis (SpA) is associated with adverse bone health outcomes. It is not known whether age at disease diagnosis is associated with osteoporosis and fracture in later life. <h3>Objectives</h3> To examine the relationship between “younger age at SpA diagnosis” and risk of osteoporosis and fractures (vertebral and low-trauma peripheral). <h3>Methods</h3> COMOSPA is a large global cross-sectional study comprising 3984 patients with SpA from 23 countries1. We evaluated the association between “younger age at SpA diagnosis” (categorised into 5-year blocks) and vertebral fracture, low-trauma peripheral fracture, and osteoporosis (t&lt;-2.5 on bone densitometry) using logistic regression. Models were adjusted for age, sex, BMI, smoking, alcohol, NSAIDs, DMARDs, biologics, steroids and vitamin D level. Subgroup analysis was performed, stratified by peripheral and/or axial joint involvement. <h3>Results</h3> Data were available for 3923 participants (64% male). Median age at SpA diagnosis was 33 (IQR 25–43) years. Younger age at SpA diagnosis was not associated with the risk of vertebral fractures in the entire cohort (OR=1.11, <i>p</i>=0.143) nor in the subgroup with axial SpA involvement, but was increased in those with peripheral arthritis (OR=1.26, <i>p</i>=0.014) indicating 26% excess risk for each 5-year younger age at time of SpA diagnosis. There was no significant association between younger age at diagnosis and the risk of low trauma peripheral fractures or spinal osteoporosis in the entire cohort or any subgroups. Younger age at SpA diagnosis was associated with higher risk of hip osteoporosis in the entire cohort (OR=1.34, <i>p</i>=0.004) and both subgroups. Femoral neck osteoporosis demonstrated similar associations (Table). <h3>Conclusions</h3> Younger age of SpA diagnosis was associated with higher risk of vertebral fracture in patients with peripheral arthritis but not axial disease in this study. Lack of association with vertebral fracture and spinal osteoporosis in axial disease may reflect difficulty in detecting spinal disease and osteoporosis in the presence of spinal pain and syndesmophytes. An association between hip osteoporosis and younger age at SpA diagnosis was noted. <h3>References</h3> Ann Rheum Dis 2016;75:1016–23. <h3>Disclosure of Interest</h3> None declared
THU0663 Serum galectin-3 binding protein is a novel predictor of venous thromboembolism in patients with systemic lupus erythematosus (SLE)
Authors: ASR Peretz, NS Rasmussen, NHH Heegaard, S Jacobsen, C Sjöwall, CT Nielsen
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> SLE patients have a marked increased risk of venous (VTE) and arterial (AT) thrombosis, which is not fully explained by traditional risk factors or the presence of anti-phospholipid antibodies. Thrombosis is a major cause of damage accrual, morbidity, and mortality in SLE. A better understanding of the pathogenesis and development of new biomarkers to identify patients at risk are needed. Recent studies link leptin and tumor necrosis factor-like weak inducer of apoptosis (TWEAK) to subclinical atherosclerosis and galectin-3-binding protein (G3BP) to type I interferon activation and a pro-thrombotic environment. <h3>Objectives</h3> To explore G3BP, interferon gamma-induced protein 10 (IP-10), soluble CD163 (sCD163), TWEAK, and leptin serum levels as predictors of venous and arterial thrombotic events, damage accrual, and all-cause mortality during long-term follow-up in a large cohort of Swedish SLE patients. <h3>Methods</h3> Baseline clinical and paraclinical data including disease activity and damage scores (SLICC) were available from 167 SLE patients. VTE (deep vein thrombosis and/or pulmonary embolism) and AT (myocardial infarction and/or cerebrovascular incident) data were available with a median follow-up period of six years. Baseline serum G3BP, IP-10, sCD163, TWEAK, and leptin were quantified using ELISA. Univariate and multivariate analyses were conducted to asses associations between the serum biomarkers and the occurrence of VTE/AT, damage accrual, and death. <h3>Results</h3> In the follow-up period 11 (7%) VTE and 12 (7%) AT events occurred. SLICC-scores increased in 79 (47%) patients, and 19 (11%) patients died. In the univariate Cox regression analysis G3BP levels were significantly associated with an increased risk of VTE (hazard ratio (HR) 1.10, 95% confidence interval (CI): 1.01–1.2, <i>P</i>=0.03). This persisted in the multivariate cox regression analyses when adjusting for age, gender, diabetes, antiphospholipid syndrome, and treatment with warfarin (HR 1.16, 95% CI: 1.04–1.31, <i>P</i>=0.01). None of the other serum biomarkers were associated with AT and VTE. No significant associations were observed between the biomarkers and changes in SLICC-scores or all-cause mortality. <h3>Conclusions</h3> Our study identifies serum G3BP as a novel independent predictor of VTE in SLE. This may improve our understanding of VTE pathogenesis in SLE and aid future VTE risk stratification and prophylaxis. Further studies are needed to translate this into clinical practice. <h3>Disclosure of Interest</h3> None declared
AB0900 Serum uric acid level variations during gout attacks are linked neither to inflammation nor to uric acid fractional excretion: a prospective study of 35 patients
Authors: V Masson Behar, C Desthieux, C Aparicio, P Manivet, T Bardin, P Richette, F Lioté, A Ostertag, H-K Ea
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Acute gout is usually associated with a decrease in serum uric acid (SUA) level but the mechanism responsible for this phenomenon remains unclear. <h3>Objectives</h3> We aimed to investigate relationships between changes in SUA level, urinary excretion of uric acid and biochemical markers during gout attack. <h3>Methods</h3> SUA, eGFR (estimated glomerular filtration rate), serum CRP level and urinary excretion of UA, expressed as fractional excretion of UA (FeUA), from 35 ULT (urate-lowering therapy)-free and diuretic-free gout patients were prospectively measured during acute gout attack (Tc) and intercritical (Tic) phase. In 11 patients, data were available after achievement of SUA target (Tt) (&lt;360 μmol/l) under ULT. Demographics data and waist circumference (WC) were collected. Data are expressed as mean ± SD. <h3>Results</h3> There were 32 men, mean age 57.9 years, mean body mass index 28.6 kg/m<sup>2</sup>, and mean waist circumference 104 cm. Overall 17.1% had type 2 diabetes, 37.1% dyslipidemia, 54.3% hypertension, 34.4% obesity, 74.3% abdominal obesity and 51.4% chronic kidney disease (CKD, 31.4% CKD 2 and 20% CKD 3–5). Gout duration was 3.9±6.7 years, 28.6% of patients had tophus and 31.4% gout arthropathy. SUA, eGFR and FeUA values were similar between Tc and Tic phases: SUA: 504.9±79.9 and 507.6±89.7 μmol/l; eGFR: 78.1±28.8 and 81.4±33.8 ml/min/1.73m<sup>2</sup>; FeUA: 4.90±2.3 and 4.45±3.3%, respectively. Moreover, the FeUA values were identical between Tt, Tic and Tc in 11 patients who achieved SUA target (296.0±37.8 μmol/l) under ULT. CRP levels were higher at Tc (44.8±69.4 mg/dL) than Tic (5.2±3.3 mg/dl) and Tt (4.6±1.2 mg/dl). While mean SUA levels were similar between Tc and Tic, SUA levels were lower in Tc than Tic in 21 patients (mean difference: 56.9±33.7 μmol/l) (figure1). In contrast, 14 patients had a SUA level higher in Tc than in Tic (mean difference: 78.6±71.5 μmol/L) (figure 1). SUA variations between Tc and Tic were not correlated with FeUA modifications in these two groups (p=0.15). Similarly, SUA and FeUA variations were not correlated with CRP variations between Tc and Tic (p=0.29 and p=0.30, respectively). <h3>Conclusions</h3> SUA levels during gout attack can be either higher or lower than SUA during intercritical phase. These variations are linked neither to inflammation level nor to FeUA. It would be interesting to assess the intestinal excretion of uric acid, xanthine oxidase activity and diet intake during these different gout phases. <h3>Disclosure of Interest</h3> None declared
MicroRNA in vivo precipitation identifies miR-151-3p as a computational unpredictable miRNA to target Stat3 and inhibits innate IL-6 production
Authors: Xiang Liu, Xiaoping Su, Sheng Xu, Huamin Wang, Dan Han, Jiangxue Li, Mingyan Huang, Xuetao Cao
Journal: Cellular and Molecular Immunology (2017)
AB0243 Serum levels of angiogenic and proinflammatory cytokines to discriminate between 6 sets of remission criteria in ra
Authors: J García Ramírez, A Cuervo, R Celis, V Ruiz-Esquide, MV Hernández, R Sanmartí, JD Cañete
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> The ideal definition of remission in RA remains to be agreed. Angiogenic factors and proinflammatory cytokines are key in RA pathogenesis. <h3>Objectives</h3> The aim of this study was to analyse serum levels differences of angiogenic and inflammatory biomarkers between SDAI, CDAI, ACR, DAS28 and sonographic remission in patients with (RA). <h3>Methods</h3> We selected patients with RA in clinical remission (DAS28-ESR&lt;2.6 for &gt;6 months). PDUS of knees and hands was performed. Serum levels of biomarkers of inflammation/angiogenesis were determined by Quantibody® Human Array. Patients were classified according to 6 sets of remission criteria: SDAI (&lt;3.3), CDAI (&lt;2.8), ACR, DAS28-ESR (&lt;2.6), Doppler (score Doppler=0) and UdAS (ultrasound defined active synovitis:no joints with SH≥2+PD) <h3>Results</h3> 60 patients with RA were collected. 76% female, aged (mean) 53 years; disease duration 110 months. 47 (76%) csDMARDs, and 27 (45%) biological therapies. At baseline, 67% of patients had PD signal and 48% fulfilled criteria for previously defined UdAS. Although patients in sonographic remission had lower levels of inflammatory biomarkers such as IL-6, IL-17 or IL-23, no significant differences were found between the 6 sets of remission criteria. Angiogenic biomarkers such as CXCL6 (0.039), ENA78 (0.007), SDF1 (0.047) and VEGF-R1 (0.025) were significantly lower in patients fulfilling CDAI remission. Patients with no PD signal (0.009) and no UdAS (0.006) had significantly lower levels of bFGF. <h3>Conclusions</h3> RA patients in CDAI remission had significantly-lower levels of angiogenic cytokines. However, no differences in serum levels of proinflammatory cytokines were found between the 6 sets of remission criteria. <h3>Disclosure of Interest</h3> None declared
Abstract 17264: Trends of Emergency Department Visits for Syncope/ Collapse in USA: Analysis of 2006-2013 National Emergency Department Sample database
Authors: Vidhu Anand, Stephen George, David Benditt, Wayne Adkisson, Selcuk Adabag
Journal: Circulation (2016)

Background:  Syncope/collapse accounts for approximately 3% of total Emergency Department (ED) visits, and available published literature indicates that about 30-40% of these individuals are admitted to hospital. To ascertain whether these hospitalization rates remain current, this study examined USA national 2006-13 trends in ED visits and hospitalizations for syncope/collapse.   Methods:  We used Nationwide Emergency Department Sample (NEDS) from 2006 through 2013 to identify syncope/collapse related ED visits using Clinical Classifications Software code 102 (includes ICD 9 codes 780.2) as the first-listed diagnosis. NEDS is the largest all-payer ED-based database with discharge data from 947 hospitals located in 30 States. NEDS includes a 20% stratified sample of U.S. hospital-based EDs, comprising nearly 134 million visits per year.   Results:  From 2006 to 2013, there was a 21% increase in ED visits with a principal discharge diagnosis of syncope/collapse (990,497 vs. 1,199,890, p   Females presented more commonly to ED with syncope/collapse than males (58% vs. 42%, p    Conclusions:  From 2006 to 2013, ED visits for syncope/collapse increased 21% in the US, but the percentage of these patients admitted to hospital after an ED visit decreased significantly. These observations may reflect the results of education designed to improve syncope/collapse risk stratification in US Emergency Departments and switch to observation status for many of these patients.   Figure 1:  Total number of ED visits and admission to the same hospital, from 2006 to 2013
AB0826 Results of bone mineral density in coeliac disease: about 30 cases
Authors: H Kchir, D Kaffel, R Zgolii, D Issaoui, H Chaabouni, H Sahli, N Maamouri, M Elleuch, MM Kchir, N Ben Mami
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> The link between Coeliac disease (CD) and low bone mass has been established in several large international studies. <h3>Objectives</h3> To determinate the prevalence and risk factors of osteopenia and osteoporosis in a Tunisian population of coeliac patients. <h3>Methods</h3> We carried a retrospective study from January 1991 to December 2015 including all cases of CD diagnosed in the departement of Gastroenterology B in Rabta9s Hospital. We retained all patients having a bone mineral density (BMD). We used the WHO criteria for the diagnosis of osteoporosis and osteopenia. <h3>Results</h3> During the period of the study, 78 cases of CD were included. Thirty among them, performed a BMD: 25 women and 5 men with an average age of 35.8 years. Malnutrtion was found in 14 patients with a BMI &lt;20Kg /m<sup>2</sup>. Smoking was found in one case. Among women, 2 were menopaused. BMD showed a low bone mass in 76,3% of patients: osteoporosis in 43.3% and osteopenia in 33.3%. The mean T score was -2.08 DS in the lumabr spine (LS) and -1DS in the Femur (F). The mean Z score was -1.66DS in LS and -0.73DS in femur. Osteoporosis was found in 13 patients: 3 men and 10 women (2 among them were menopaused). The research of risk factors of osteoporosis found a smoking (N=1), and an associated autoimmune disease in 5cases: A diabetes Mellitus in 3 patients, and an autoimmune hepatitis an Sjogren Syndrome in 1 case. Finally, a marked villous atrophy was associated to osteoporosis in 9 cases. <h3>Conclusions</h3> Our study showed that approximately ¾ of coeliac patients had a low bone mass. Osteoporosis was found in 33% of our patients and was associated to a marked villous atrophy. <h3>Disclosure of Interest</h3> None declared
Structurally Novel Antiestrogens Elicit Differential Responses from Constitutively Active Mutant Estrogen Receptors in Breast Cancer Cells and Tumors
Authors: Yuechao Zhao, Mary J. Laws, Valeria Sanabria Guillen, Yvonne Ziegler, Jian Min, Abhishek Sharma, Sung Hoon Kim, David Chu, Ben Ho Park, Steffi Oesterreich, Chengjian Mao, David J. Shapiro, Kendall W. Nettles, John A. Katzenellenbogen, Benita S. Katzenellenbogen
Journal: Cancer Research (2017)

Abstract Many estrogen receptor α (ERα)–positive breast cancers develop resistance to endocrine therapy via mutation of ERs whose constitutive activation is associated with shorter patient survival. Because there is now a clinical need for new antiestrogens (AE) against these mutant ERs, we describe here our development and characterization of three chemically novel AEs that effectively suppress proliferation of breast cancer cells and tumors. Our AEs are effective against wild-type and Y537S and D538G ERs, the two most commonly occurring constitutively active ERs. The three new AEs suppressed proliferation and estrogen target gene expression in WT and mutant ER-containing cells and were more effective in D538G than in Y537S cells and tumors. Compared with WT ER, mutants exhibited approximately 10- to 20-fold lower binding affinity for AE and a reduced ability to be blocked in coactivator interaction, likely contributing to their relative resistance to inhibition by AE. Comparisons between mutant ER–containing MCF7 and T47D cells revealed that AE responses were compound, cell-type, and ERα-mutant dependent. These new ligands have favorable pharmacokinetic properties and effectively suppressed growth of WT and mutant ER–expressing tumor xenografts in NOD/SCID-γ mice after oral or subcutaneous administration; D538G tumors were more potently inhibited by AE than Y537S tumors. These studies highlight the differential responsiveness of the mutant ERs to different AEs and make clear the value of having a toolkit of AEs for treatment of endocrine therapy–resistant tumors driven by different constitutively active ERs. Cancer Res; 77(20); 5602–13. ©2017 AACR.
AB1159 High dose glucocorticoids as a risk factor of sigmoid diverticulitis perforations in autoimmune diseases
Authors: T Kuranobu, M Ishitoku, T Tokunaga, Y Yoshida, S Hirata, T Nojima, E Sugiyama
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> It has been reported that glucocorticoids (GCs) and non-steroidal anti-inflammatory drugs (NSAIDs) might increase sigmoid diverticulitis perforations (SDPs) for rheumatoid arthritis patients, however, there are few previous reports referring to the relationship between SDPs and GCs in patients with systemic autoimmune diseases. We investigate relationship between SDPs and GCs in patients used GCs for not only rheumatic patients but also other autoimmune disease9 sufferer. SDPs and GCs <h3>Objectives</h3> To describe development of SDPs during high dose GC (over PSL 0.8mg/kg equivalent) therapy for systemic autoimmune diseases in our department, additionally reviewing previous reports with regard to the relationship between SDPs and GCs. <h3>Methods</h3> 187 patients hospitalized in our department from April 2015 to December 2016 were retrospectively reviewed. <h3>Results</h3> Among 187 patients, 61 took high dose GCs, 29 took moderate dose GCs (0.5–0.6mg/kg PSL equivalent), 53 took low dose (less than 0.5mg/kg PSL equivalent), and 29 didn9t take GCs. Four patients out of 61 who took high dose GCs developed SDPs (table). Nobody developed SDPs in moderate, low and not any dose GCs group. Case 1–3 took NSAIDs. Case 2 received mPSL pulse therapy (mPSL 1 g x 3 days). Case 1 and 2 developed SDPs within 3 months from initiating GCs. Case 1 recurred SDPs at 17 and 63 months from initiating GCs. Case 2 was prescribed Tacrolimus as a concurrent medication. All four patients were operated to remove the perforated segment, and case 2 and 4 were created artificial anus. Although they were clinically diagnosed as SDPs only case 4 clarified perforation in pathological findings. <h3>Conclusions</h3> We should take care of developing SDPs in patients described high dose GCs. <h3>References</h3> Mpofu S, Mpofu CM, Hutchinson D, Maier AE, Dodd SR, Moots RJ. Steroids, non-steroidal anti-inflammatory drugs, and sigmoid diverticular abscess perforation in rheu- matic conditions. Ann Rheum Dis 2004; 63: 588–590. Humes DJ, Fleming KM, Spiller RC, West J. Concurrent drug use and the risk of perforated colonic diverticular dis- ease: a population-based case-control study. Gut 2011; 60: 219–224. <h3>Disclosure of Interest</h3> None declared
THU0243 Can the increase of lobules / foci ratio be histopathological evidence of primary sjÖgren's syndrome
Authors: B Ünal, V Yazısız, GÖ Elpek, M Göçer, ME Terzioğlu
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Minor salivary gland biopsy from the lip region is commonly used for primary Sjögren9s syndrome (SS) diagnosis. It is accepted that changes of histopathology is the most important component of diagnostic criteria. In this study, we analyzed the relationship between histopathological changes and laboratory findings/clinical features in SS patients and control group. <h3>Objectives</h3> The aim of this study was to determine the histopathological changes in minor salivary tissue for SS diagnosis <h3>Methods</h3> A total of 69 minor salivary gland biopsies (29 Sjögren9s syndrome and 40 controls) were included in the study. Biopsies were evaluated by a blind pathologist unaware of the diagnosis. Histopathological findings were noted as ductal dilatation, fat tissue percentage (&lt;10% or &gt;10%), acinar atrophy, ductal/ acinar ratio and lobules/foci ratio. It was evaluated whether there was a relationship between histological changes and age, gender, ANA, anti-SSA, anti-SSB, RF and Chisholm scores. <h3>Results</h3> The lobules/foci ratio of patients with Sjögren9s syndrome was significantly higher than the control group (p&lt;0.001). The cutoff value of the lobules/foci ratio for SS diagnosis was 0.8. Furthermore, there was a significant correlations between the lobules/foci ratio greater than 0.8 and antibodies (ANA, RF, anti-Ro) positivity and Chisholm score (p&lt;0.01). Other histopathological findings such as ductal dilatation, fat tissue percentage, acinar atrophy, and ductal/atherine ratio do not distinguish SS from non-SS. <h3>Conclusions</h3> The results of this study revealed that only the lobules/foci ratio from histopathological changes has a strong relation with SS diagnosis. It can be important for pathologists to distinguish SS. <h3>Disclosure of Interest</h3> None declared
Headache and papilloedema in a 10 year old
Authors: Anan Shtaya, Bassam Dabbous
Journal: BMJ (2017)

A 10 year old girl described intense headaches at the front of her head, which had been coming and going since she banged her head two months earlier. She also described feeling sick with the headaches, and had vomited on several occasions. On examination, she had papilloedema, otherwise neurological examination was normal. She had a computed tomography (CT) scan of the head (fig 1A⇓) followed by magnetic resonance imaging (MRI) of the brain (fig 1B⇓). What is the relevant finding?



Fig 1  Axial computed tomography …
SAT0274 Urinary vitamin d-binding protein as a biomarker for lupus nephritis
Authors: DJ Go, JY Lee, MJ Kang, IA Choi, EY Lee, EB Lee, E Yi, YW Song
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Lupus nephritis (LN) is a major complication of systemic lupus erythematosus (SLE). However, conventional biomarkers for assessing renal disease activity are imperfect in predicting clinical outcomes associated with LN. <h3>Objectives</h3> The aim of this study is to identify urinary protein biomarkers that reliably reflect the disease activity or predict clinical outcomes. <h3>Methods</h3> A quantitative proteomic analysis, using liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS), was performed to identify protein biomarker candidates that can differentiate between SLE patients with and without LN. Selected biomarker candidates were further verified using urine samples from a larger cohort of SLE patients (n=121) by enzyme-linked immunosorbent assay (ELISA) to investigate their predictive values for LN activity measure. Furthermore, association between urinary level of selected panel of potential biomarkers and prognosis of LN was assessed with a 4-year follow-up study of renal outcomes. <h3>Results</h3> From proteomic assay, vitamin D binding protein (VDBP), transthyretin (TTR), retinol binding protein 4 (RBP4) and prostaglandin D synthase (PTGDS) were selected as candidates for quantification. These proteins were significantly elevated in SLE patients with LN, especially in patients with active LN (n=21). Among them, VDBP well correlated with severity of proteinuria (rho =0.661, P&lt;0.001) and renal SLE disease activity index (renal SLEDAI) (rho =0.520, P&lt;0.001). In the 4-year follow-up, VDBP was a significant risk factor (hazard ratio 9.627, 95% CI 1.698 to 54.571, P=0.011) for the development of proteinuric flare (randum urine protein/creatinine ratio &gt;1.0) in SLE patients without proteinuria (random urine protein/creatinine ratio &lt;0.5) (n=100) after adjustments of multiple confounders. <h3>Conclusions</h3> Urinary VDBP correlated with proteinuria and renal SLEDAI, and predicted the development of proteinuria. <h3>Disclosure of Interest</h3> None declared