tbuckley/cabot-search huggingface dataset:
AB0937 Dupuytren's contracture: 15 years of experience with 36 cases
Authors: H Mouanaa, M Jguirim, A Arfa, A Farhat, M Brahim, A Mhenni, Z Saoussen, I Bejia, M Touzi, N Bergaoui
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Dupuytren9s contracture is characterized by thickening and retraction of the palmar aponeurosis due to fibroblastic proliferation leading to progressive and irreducible fingers9 flexion. Dupuytren9s contracture appears to be a disease with poor clinical symptomatology and the therapeutic progress, in particular the needle aponeurotomy, continues to increase. <h3>Objectives</h3> We propose to describe the epidemiological, clinical and therapeutic characteristics- particularly the needle fasciotomy- of Dupuytren9s contracture diagnosed and treated in our Rheumatology department. <h3>Methods</h3> This is a retrospective descriptive study that collected patients with Dupuytren9s disease over a 15-year period from 2001 to 2016. <h3>Results</h3> Thirty-six patients were collected. The mean age was 63±10 years (46 years, 83 years) and the sex ratio was 5. 34% of the patients were manual workers, of whom 42% were masons, 25% were farmers and 17% were carpenters. 8% Of longshoremen and 8% of dressmakers. The personal history was diabetes in 63% of cases, of which 26% were unbalanced, hypertension in 31% of cases and hypercholesterolemia in 14% of cases. 6% of patients were epileptic. 23% of patients were ethyl and 13% were smokers. 6% had an associated Leddherhose disease. 9% of our patients had a family history of Dupuytren9s disease. The mean time to diagnosis was 60 months [03 months to 180 months]. The clinical examination showed an exclusive involvement of the left hand in 22% of cases, right hand in 12% of cases and bilateral involvement in 66% of cases. The fingers affected were: 59% the ring finger, 49% the little finger, 23% the middle finger, 12% the index and 5.5% the inch, in order of frequency of mention. The stages of Dupuytren9s disease at their discovery were as follows: stage 4 (25%), stage 3 (34%), stage 2 (24%) and stage 1 (17%). Skin examination showed that 58% of the skin was inflicted and 42% of the skin was soft. From a therapeutic point of view, 86% of the patients benefited from a needle aponevrotomy with a good progression in 97% and a recurrence in 8% of the cases. In all stages combined, the average postoperative therapeutic gain was 0.83 stage at the Left hand and 1.43 stage at the right. <h3>Conclusions</h3> The Dupuytren9s contracture is the object of a scientific subject whose wealth grows exponentially. These range from the paternity of his first description, to the place of the last therapeutic modalities. <h3>Disclosure of Interest</h3> None declared
FRI0070 Angiotensin II type 2 receptor (AT2R) is overexpressed in rheumatoid arthritis and osteoarthritis synovium and increases steadily with inflammatory stimuli: a potential new target for pain and anti-inflammatory therapies
Authors: R Terenzi, M Manetti, I Rosa, E Romano, F Galluccio, S Guiducci, L Ibba-Manneschi, M Matucci-Cerinic
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Despite increasing evidence suggesting that angiotensin II type 2 receptor (AT2R) antagonism might be a feasible strategy for the treatment of chronic inflammation and pain, no study has yet analyzed the synovial expression of AT2R. <h3>Objectives</h3> To investigate the expression of AT2R in rheumatoid arthritis (RA) and osteoarthritis (OA) synovium and its possible modulation in fibroblast-like synoviocytes (FLS) by proinflammatory stimuli. <h3>Methods</h3> The expression of AT2R in RA and OA synovium was investigated by immunohistochemistry. AT2R expression in synovial T cells, B cells, macrophages and FLS was assessed by double immunofluorescence. FLS were isolated from healthy (H), OA and RA synovium and treated with tumor necrosis factor (TNF)-α and interleukin (IL)-1β, alone or in combination. Immunocytochemistry and Western blotting were performed to study AT2R expression in cultured FLS. <h3>Results</h3> RA synovium showed stronger AT2R immunostaining than OA synovium in the lining and sublining layers. In RA synovium, AT2R was strongly expressed in CD3+ T cells, CD20+ B cells, CD68+ macrophages and vimentin+ FLS. High levels of AT2R were found in OA-FLS and RA-FLS at baseline, while AT2R expression was negligible in basal H-FLS. AT2R expression was higher in RA-FLS than OA-FLS. Treatment with TNF-α and IL-1β was able to foster the expression of AT2R not only in OA-FLS and RA-FLS, but also in H-FLS. <h3>Conclusions</h3> AT2R is strongly expressed in different cell types of the inflamed synovium and proinflammatory stimuli may foster the expression of AT2R in FLS. AT2R might represent a novel potential therapeutic target in chronic arthritides. <h3>Disclosure of Interest</h3> None declared
Rotavirus vaccine response correlates with the infant gut microbiota composition in Pakistan
Authors: Vanessa Harris, Asad Ali, Susana Fuentes, Katri Korpela, Momin Kazi, Jacqueline Tate, Umesh Parashar, W. Joost Wiersinga, Carlo Giaquinto, Carolina de Weerth, Willem M. de Vos
Journal: Gut Microbes (2017)

Rotavirus (RV) is the leading cause of diarrhea-related death in children worldwide and ninety-five percent of rotavirus deaths occur in Africa and Asia. Rotavirus vaccines (RVV) can dramatically reduce RV deaths, but have low efficacy in low-income settings where they are most needed. The intestinal microbiome may contribute to this decreased RVV efficacy. This pilot study hypothesizes that infants' intestinal microbiota composition correlates with RVV immune responses and that RVV responders have different gut microbiota as compared to non-responders. We conducted a nested, matched case-control study comparing the pre-vaccination intestinal microbiota composition between 10 6-week old Pakistani RVV-responders, 10 6-week old Pakistani RVV non-responders, and 10 healthy Dutch infants. RVV response was defined as an Immunoglobulin A of ≥20 IU/mL following Rotarix™(RV1) vaccination in an infant with a pre-vaccination IgA<20. Infants were matched in a 1:1 ratio using ranked variables: RV1 dosing schedule (6/10/14; 6/10; or 10/14 weeks), RV season, delivery mode, delivery place, breastfeeding practices, age and gender. Fecal microbiota analysis was performed using a highly reproducible phylogenetic microarray. RV1 response correlated with a higher relative abundance of bacteria belonging to Clostridium cluster XI and Proteobacteria, including bacteria related to Serratia and Escherichia coli. Remarkably, abundance of these Proteobacteria was also significantly higher in Dutch infants when compared to RV1-non-responders in Pakistan. This small but carefully matched study showed the intestinal microbiota composition to correlate with RV1 seroconversion in Pakistan infants, identifying signatures shared with healthy Dutch infants.
AB0410 The interplay between C3 and C4 and disease activity in patients affected by rheumatoid arthritis during treatment with ANTI-IL6 receptor
Authors: P Conigliaro, P Triggianese, MS Chimenti, I Duca, B Kroegler, R Perricone
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> The complement system (CS) is involved in the pathogenesis of rheumatoid arthritis (RA). Evidence reported that high C3 levels C3 in RA patients might reflect a pro-inflammatory status and represent a negative prognostic factor for TNF-inhibitors therapy. <h3>Objectives</h3> We evaluated CS in a cohort of RA patients treated with tocilizumab (TCZ) to explore whether there was any correlation between CS and both disease activity and response to therapy. <h3>Methods</h3> Consecutive outpatients affected by RA who started TCZ treatment i.v. at the Rheumatology Unit of "Policlinico Tor Vergata" in Rome (Italy) were enrolled (n=25) (Table I). We included 25 healthy subjects as controls. Disease activity was assessed by using DAS28 ESR-based while clinical response to therapy by EULAR response criteria. Peripheral blood samples were obtained from all patients at the time of each infusion. Laboratory assessment included ESR, CRP, RF, ACPA, C3, C4, CH50 assay. Clinical and laboratory data were registered at baseline (T0), after 1 (T1), 3 (T3), 6 (T6), 9 (T9), and 12 (T12) months from the beginning of the TCZ treatment. <h3>Results</h3> At baseline, both C3 and C4 were significantly higher in RA than in controls (Table 1). No difference in C3 and C4 resulted between ACPA positive and ACPA negative patients during the follow up. ESR, CRP and DAS28 levels were significanlty reduced at T1, T3, T6, T9, and T12 with the respect to T0 (Figure 1A-C). C3 levels were significantly reduced at T3, T6, and T9 with the respect to T0 while C4 levels were significantly reduced at T3, T6, T9, and T12 with the respect to T0 (Figure 1D-E). Positive correlations resulted between DAS28 and both C3 and C4 at T1 and T3 (Figure 1F-I). C3 and C4 were directly related with ESR at T1 (C3: P 0.002; C4: P 0.005), T3 (C3: P 0.04; C4: P 0.03), and T6 (C3: P&lt;0.0001; C4: P 0.002) and with CRP at T1 (C3: P 0.03; C4: P 0.01) and T6 (C3: P&lt;0.0001; C4: P 0.03). When stratifying patients in accordance with the EULAR response to therapy, C3 decreased significantly in responders than in no-responders at T1; moreover, responders showed lower levels of both C3 and C4 at T1 and T3 with the respect to T0 (Figure 1L-O). <h3>Conclusions</h3> In RA patients, treatment with TCZ is able to reduce C3 and C4 levels in an early and substained way. The disease activity is directly related with the reduction of C3 and C4 serum levels. RA patients with a good/moderate clinical response show significantly lower C3 and C4 levels than no-responder patients. Our preliminary data suggest that C3 and C4 can be a reliable marker of both the disease activity and the response to therapy in RA patients treated with TCZ. <h3>Disclosure of Interest</h3> None declared
AB0987 The relationship between anti-interleukin-1 therapies and mefv gene mutations in familial mediterranean fever patients: a single center experience
Authors: ME Derin, S Gültekin, M Şahin, A Şahin
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Familial Mediterranean fever (FMF) is an autoinflammatory disease characterizing recurrent self-limiting attacks of inflammation mainly placed in serosal surfaces of the body with fever (1). Colchicine is an important weapon of the humanity in FMF treatment yet. However, the puzzle of inflammation was solved, and so, inflammasome complex and interleukin-1 were discovered. Eventually, new era started with anti-interleukin-1 agents in colchicine resistant and/or intolerant FMF patients (2). <h3>Objectives</h3> The aim of this study is to evaluate the effectiveness of anti-interleukin-1 (anti-IL-1) agents on the characteristics of attacks, the adverse effects associated with anti-IL-1 treatment, and relation between therapy and MEFV gene mutations in 23 FMF patients with resistant and/or intolerant to colchicine. <h3>Methods</h3> Between January 2015 and December 2016, twenty-three-FMF patients that following-up at Cumhuriyet University Medical Faculty Rheumatology-Internal Medicine Department were included in to the study. Anakinra (69,6%), and canacinumab (30,4%)] were used in 23 FMF patients. 20 cases were resistant to colchicine, 3 were intolerant to colchicine. <h3>Results</h3> The median age of the patients was 28 years,(18–54) and the median age at diagnosis was 20 years (3–50). Of the FMF patients, nine (39.1%) were female and fourteen (60.9%) were male. The distribution of MEFV gene mutation frequencies in the FMF patients was no mutation in one (4,3.%) patient, M694V heterozygous in nine (39,1%), M694V homozygous in 7 (30,4%), E148Q heterozygous in one (4,3%), and compound heterozygous mutation in 3. (13%) patients. 16 patients used anakinra (100mg/day) for 6 mounths (median) and 7 used canacinumab (150mg/2 months) for 3 mounths (median). Four of 7 patiens were resistant to anakinra. After a median follow up 6 months overall clinical response [no attack (18 patients) or decreased frequency of attacks (5 patients)] was %100. In an FMF patient with no mutation, his brother and mother had FMF with no mutations on MEFV gene. We achieved good clinical and laboratory responses in the patient by canacinumab. <h3>Conclusions</h3> Anti-IL-1 agents can be got involved in a new place safely and effectively in FMF patients along with colchicine. In addition, whole gene analysis should be done in refractory FMF patients with no mutations in order to could investigate new mutations, epigenetic mechanisms or other unexplained reasons. <h3>References</h3> Ben-Chetrit E, Touitou I. Familial Mediterranean Fever in the world. Arthritis Rheum 2009; 61:1447–1453. Özdoğan H, Ugurlu S. The emerging treatments in Familial Mediterranean fever. In: Gattorno M, editor. Familial Mediterranean Fever, 1st edition, Switzerland: Springer; 2015:137–157. <h3>Disclosure of Interest</h3> None declared
SP0005 Looking back at 70 years of eular and 30 years of hp involvement: a rehabilitation perspective
Authors: T Vliet Vlieland
Journal: Annals of the Rheumatic Diseases (2017)

The medical treatment of people with rheumatic and musculoskeletal diseases (RMDs) has improved enormously over the past decades. As medical treatment is not completely successful or available for all rheumatic conditions or individual patients, and the demands society imposes on people to participate fully are increasing, there is a substantial proportion of people with RMDs who have functional disabilities. Health professionals (HPs) play an essential role in the management of people with RMDs with disabilities by enabling to reach and maintain their optimal physical, sensory, intellectual, psychological and social functional levels. They provide people with the tools they need to attain independence and self-determination. As such, their contribution is in line with the World Health Organisation definition of rehabilitation [http://www.who.int/topics/rehabilitation/en/]. An important feature of rehabilitation is its multidisciplinarity. Over the past decades, it has been more and more acknowledged that HPs9 role in the management of people with RMDs concerns a team effort rather than the summation of single interventions by individual HPs or specific professions. This view is reflected in multiple guidelines and standards of care for the clinical management of RMDs, where the need for people with RMDs to have access to a multidisciplinary team of HPs is underlined. The acknowledgement of the importance of the team of HPs runs in parallel with developments in the organization and activities of HPs within EULAR over the past years. In connection with EULAR, there is a growing network of HPs from multiple professions across Europe. By working together, and collaborating with patients and rheumatologists and other physicians, EULAR HPs have achieved multiple milestones with respect to the quality of clinical care, education, and research over the past years and are equipped to encounter future challenges. <h3>Disclosure of Interest</h3> None declared
Acquisition of wild-type HIV-1 infection in a patient on pre-exposure prophylaxis with high intracellular concentrations of tenofovir diphosphate: a case report
Authors: Elske Hoornenborg, Maria Prins, Roel C A Achterbergh, Lycke R Woittiez, Marion Cornelissen, Suzanne Jurriaans, Neeltje A Kootstra, Peter L Anderson, Peter Reiss, Henry J C de Vries, Jan M Prins, Godelieve J de Bree
Journal: The Lancet HIV (2017)
SAT0372 Clinical and serological associations of autoantibodies to BICD2 as a novel marker for systemic sclerosis
Authors: M Mahler, C Bentow, J Milo, M Hudson, H-D Zucht, P Budde, D Wirtz, J Schulte-Pelkum, M Choi, M Fritzler
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Anti-nuclear antibodies (ANA), which are present in approximately 90% of systemic sclerosis (SSc) patient9s sera, play an important role in establishing the diagnosis and predicting prognosis of SSc. Recently, a novel autoantibody has been described in SSc patients targeting Cytoskeleton-Like Bicaudal D Protein Homolog 2 (BICD2). <h3>Objectives</h3> The aim of this study was to assess the prevalence and titers of anti-BICD2 antibodies in SSc and controls and to study the clinical associations of this new antibody. <h3>Methods</h3> A total of 502 samples from SSc patients enrolled in the Canadian Scleroderma Research Group (CSRG) cohort were included in this study. Clinical associations were assessed either as anti-BICD2 antibody positivity with and without other autoantibodies present using 451 SSc patients with complete dataset. Autoantibodies to several scleroderma-related autoantibodies were detected using commercial or research use only kits (Inova Diagnostics, San Diego, USA). P-values below 0.05 were considered significant. <h3>Results</h3> The sensitivity and specificity of anti-BICD2 antibodies were determined as 22.1% and 99.0%, respectively. Receiver operating characteristic (ROC) analysis showed an area under the curve of 0.79 (95% CI 0.75–0.84). The likelihood (LR) and odds ratios (OR) were 17.7 (LR+), 0.8 (LR-) and 20.4 (OR). The prevalence of these autoantibodies was equally distributed between limited and diffuse form of SSc (22.8% and 24.0%). When SSc patients without the classification criteria markers anti-Scl-70, anti-Centromere and anti-RNA Pol III (n=184) were compared with controls, similar performance was obtained as seen in the entire cohort. Results are summarized in table 1 below. Several statistically relevant clinical associations were found for anti-BICD2 as summarized in table 2 below. <h3>Conclusions</h3> Our data confirm the presence of anti-BICD2 antibodies in SSc patients that may help to differentiate SSc from other systemic autoimmune rheumatic diseases and to stratify SSc patients into more defined subforms of the disease. <h3>Disclosure of Interest</h3> M. Mahler Employee of: Inova Diagnostics, C. Bentow Employee of: Inova Diagnostics, J. Milo Employee of: Inova Diagnostics, M. Hudson: None declared, H.-D. Zucht Employee of: Protagen, P. Budde Employee of: Protagen, D. Wirtz Employee of: Protagen, J. Schulte-Pelkum Employee of: Protagen, M. Choi: None declared, M. Fritzler: None declared
AB0057 The role of growth differentiation factor (GDF)-15 and transforming growth factor (TGF)-β in the development of pulmonary fibrosis
Authors: V Yazisiz, S Oygen, M Çavuşoğlu, M Kahraman, EG Gök, S Karahan, I Uçar, ME Terzioğlu
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> The pathogenesis of pulmonary fibrosis is not fully understood and it is thought to develop secondary to inflammation. The main cause of pulmonary fibrosis is considered to be interstitial lung disease (ILD), which can be associted with connective tissue disorders (CTD). <h3>Objectives</h3> The aim of this study was to investigate serum GDF-15 and TGF-β levels in patients with diagnosis of CTD associated with ILD. <h3>Methods</h3> A total of 103 adult patients (19 rheumatoid arthritis, 18 Sjögren9s syndrome, 32 systemic sclerosis, 3 systemic lupus erythematosus and 31 healthy controls) were included in the study. Pregnant, acute coronary syndrome, previous myocardial infarction and/or stroke history, heart failure and malignancy were excluded. Serum GDF-15 and TGF-β levels were studied by ELISA method in peripheral blood samples. <h3>Results</h3> There were 44 patients with CTD-ILD, 28 patients without ILD and 31 healthy controls. The age and gender distributions of participants in all three groups were not different. Serum TGF-β and GDF-15 levels in patients with CTD-ILD and CTD without ILD were significantly higher than healthy controls (respectively, 3.05±0.26, 3.05±0.22, 1.39±0.33 pg/ml, p&lt;0.001 for TGF-β and 1.17±0.17, 1.12±0.05, 0.95±0.21 pg/ml, p&lt;0.001 for GDF-15). There were no statistically different from patients with ILD and without ILD for both TGF-β (p:0.864) and GDF-15 levels (p:0.146) in CTD. Also, GDF-15 and TGF-β levels of patients with systemic sclerosis were not different from other CTD9s. <h3>Conclusions</h3> Our findings indicate that TGF-β and GDF-15 are increased in CTD patients but, they are not a specific markers for CTD-ILD <h3>Disclosure of Interest</h3> None declared
FRI0065 Helminthes based novel compound, tuftsin-phosphorylcholine (TPC) ameliorates established murine arthritis
Authors: T Bashi, J Lachnish, M Fridkin, Y Shoenfeld, M Blank
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> In areas where helminthes infections are common, autoimmune diseases are rare. Treatment with helminthes or their ova, improved clinical findings of several autoimmune diseases. Based on the helminthes biological activity, a novel chimeric be-specific molecule was synthetized of tuftsin-phosphoryl-choline (PC)-TPC. <h3>Objectives</h3> To study TPC treatment in established collagen induced arthritis (CIA) mice, and the mechanism of activity. <h3>Methods</h3> Arthritis was induced in DBA male mice by immunization with collagen emulsified in TB-mycobacteria at the tail base. Boost was given 3 weeks later. Treatment with TPC started when the clinical score was 2. Cytokines were measure in culture-fluid of splenocytes in-vitro. T regulatory cells and B regulatory cells were measured by FACS. TPC effect on TLR4 expression was studied using HEKTM-mTLR4 cells system and its inhibitor. M1 shift to M2 was performed in RAW macrophages differentiated to M1 by PMA followed by LPS. TPC was added and IL-6, TNFalpha, IL-10 were tested by ELISA. <h3>Results</h3> Starting TPC treatment of CIA mice after disease establishment, had a significant lower arthritis score in comparison with control vehicle subjected mice (i.e. TPC-6.8±0.8 vs vehicle-13.8±0.45; p&lt;0.0001). Joints staining revealed normal joint structure in TPC treated mice, whereas, control mice treated with PBS, PC or tuftsin had severe inflamed joints. Likewise, TPC enhanced anti-inflammatory response by enhanced IL-10 secretion, reduced pro-inflammatory cytokines secretion (IL-1β, IL-17, IL-6, and TNF-α) (p&lt;0.001). Furthermore, TPC induced expansion of splenic CD4+CD25+FOXP3+ T regulatory cells (Tregs) and IL-10+CD5+CD1d+ B regulatory cells (Bregs). The mechanism underling the TPC related immunomodulatory activity was attributed to its bi-specific activity: a) Shift of Raw cells macrophages from pro-inflammatory macrophages M1 to anti-inflammatory M2 secreting anti- IL-10 (p&lt;0.001), through the tuftsin part of TPC. b) TPC inhibited significantly TLR4 expression by HEKTM-mTLR4 cells (p&lt;0.02) <i>via</i> the phosphorylcholine end. Our data indicated that TPC significantly ameliorated established CIA by anti-inflammatory immunomodulatory activity. <h3>Conclusions</h3> Our data may lead to a novel bi-specific self small molecule for therapy of patients with advanced RA. <h3>Disclosure of Interest</h3> None declared
Roles for Innate Immunity in Combination Immunotherapies
Authors: Kelly D. Moynihan, Darrell J. Irvine
Journal: Cancer Research (2017)

Abstract Immunity to infectious agents involves a coordinated response of innate and adaptive immune cells working in concert, with many feed-forward and regulatory interactions between both arms of the immune system. In contrast, many therapeutic strategies to augment immunity against tumors have focused predominantly on stimulation of adaptive immunity. However, a growing appreciation of the potential contributions of innate immune effectors to antitumor immunity, especially in the context of combination immunotherapy, is leading to novel strategies to elicit a more integrated immune response against cancer. Here we review antitumor activities of innate immune cells, mechanisms of their synergy with adaptive immune responses against tumors, and discuss recent studies highlighting the potential of combination therapies recruiting both innate and adaptive immune effectors to eradicate established tumors. Cancer Res; 77(19); 5215–21. ©2017 AACR.