tbuckley/cabot-search huggingface dataset:
FRI0627 Ultrasound hand examination is more sensitive in diagnosing hand osteoarthritis than conventional radiography: comparison between different ultrasonographic scores
Authors: S Hussain, P Sivakumaran, C Ciurtin
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Hand osteoarthritis (OA) diagnosis is based on a combination of clinical, imaging features and assessment of risk factors, together with clinical associations and outcomes (1). In a real-life context, clinicians face difficulty in differentiating between OA and other hand arthropathies, particularly when the clinical examination is equivocal (e.g. no obvious bony enlargement with the characteristic distribution for hand OA). <h3>Objectives</h3> This is the first study to investigate the usefulness of a standardised ultrasound (US) examination protocol for hand joints in diagnosing hand osteoarthritis (OA) and the correlations between several US scores and clinical, inflammatory and radiographic parameters, aiming to explore which type of investigations are the most useful for diagnosing hand OA. <h3>Methods</h3> We conducted a cross-sectional study including 62 patients, ultimately diagnosed with hand OA based on the ACR diagnosis criteria (2). We compared the 34 joint score of the hand, with smaller, pre-defined joint scores including two scores of 22 and 12 joint each, and another 10 and 6 joint scores for OA. We correlated the US findings with radiographic scores (2108 joints). <h3>Results</h3> Radiographic osteophyte scores correlated very well with the predefined US scores detailed above (R=0.381 to 0.645, P&lt;0.05), despite having a low sensitivity for detection of osteophytes (58.6%), and an even lower sensitivity for detection of erosions (38.4%) when compared with the 34 joint US score. There was a good correlation between different US scores (R =0.53 to 0.97, P&lt;0.05), apart from the 6 joint score excluding the proximal interphalangeal joints (R= -0181 to 0.207, P&gt;0.05). <h3>Conclusions</h3> US examination of the hands can facilitate the diagnosis of hand OA in patients who do not fulfil the ACR criteria, by identifying the presence of osteophytes with the particular distribution and number required for diagnosis in a proportion of patients that was three times higher than that of patients diagnosed based on clinical examination and hand radiography alone. <h3>References</h3> Zhang W, Doherty M, Leeb BF, Alekseeva L, Arden NK, Bijlsma JW, et al. EULAR evidence-based recommendations for the diagnosis of hand osteoarthritis: report of a task force of ESCISIT. Annals of the rheumatic diseases. 2009 Jan;68(1):8–17. PubMed PMID: 18250111. Epub 2008/02/06. eng. Altman R, Alarcon G, Appelrouth D, Bloch D, Borenstein D, Brandt K, et al. The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hand. Arthritis and rheumatism. 1990 Nov;33(11):1601–10. PubMed PMID: 2242058. Epub 1990/11/01. eng. <h3>Acknowledgements</h3> S. Hussain and P. Sivakumaran contributed equally to this study. <h3>Disclosure of Interest</h3> None declared
Nationwide Coverage and Cost-Sharing for PCSK9 Inhibitors Among Medicare Part D Plans
Authors: Dhruv S. Kazi, Christine Y. Lu, Grace A. Lin, Colette DeJong, R. Adams Dudley, Randi Chen, Chien-Wen Tseng
Journal: JAMA Cardiology (2017)

Gregg C. Fonarow, MD; Anthony C. Keech, MD; Terje R. Pedersen, MD; Robert P. Giugliano, MD, SM; Peter S. Sever, PhD, FRCP; Peter Lindgren, PhD; Ben van Hout, PhD; Guillermo Villa, PhD; Yi Qian, PhD; Ransi Somaratne, MD; Marc S. Sabatine, MD, MPH
FRI0261 Skin cancer in a cohort of systemic lupus erythematosus
Authors: M Taraborelli, C Genitori, I Cavazzana, M Fredi, A Tincani, P Calzavara Pinton, F Franceschini
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Conflicting results about the prevalence of skin cancer in Systemic Lupus Erythematosus (SLE) have been reported in the literature [1,2]. <h3>Objectives</h3> The aim of this study was to retrospectively evaluate the prevalence of malignancies, with a particular focus on skin cancers, in a cohort of SLE patients followed in a single Center. <h3>Methods</h3> All the SLE patients classified according to the ACR and SLICC criteria, attending the Rheumatology and Clinical Immunology Unit of Spedali Civili, Brescia, were retrospectively evaluated. Clinical and laboratory data were obtained from clinical charts. Diagnoses of skin cancers (melanoma and non-melanoma: basalioma, squamous cell carcinoma) and other malignancies were recorded together with the time elapsed from diagnosis of SLE. Univariate analysis was performed to compare characteristics of patients with (K+) and without (K-) cancer. We also compared the prevalence of cancer in our population to that reported in the italian general population (from the Italian National Institute of Statistics, ISTAT, report 2014). <h3>Results</h3> In a cohort of 511 SLE patients (92% females,95% caucasian) regularly followed from 1972 to 2016 (mean age at diagnosis 31 years±13 and median follow-up 12 years, range 1–40) we detected 51 cases (9,9%) with a history of malignancy: melanoma was reported in 3 (0.5%), non melanoma skin cancer (NMSC) in 11 (2%) and other malignancies in 38 cases (7.4%). Table I reports the comparison between patients with and without cancer. Patients with cancer, as well as cases with NMSC and non cutaneous malignancies, showed a higher age at disease onset (p&lt;0.0001; p=0.002 and p&lt;0.0001 respectively) and higher SLE damage (p&lt;0.0001; p=0.019 and p&lt;0.0001 respectively) compared with patients without malignancies. Patients with melanoma showed the same age at SLE onset, but a higher prevalence of discoid lupus (p&lt;0.0001) and oral ulcer history (p=0.02). No difference in serological SLE features or in disease activity were detected between groups. The prevalence of melanoma in our cohort (0.5%) was only slightly higher than the one reported in the northern Italian general population (0.2%), while the prevalence of NMSC (2%) resulted to be significantly higher than that reported in the same population (prevalence of spinocellular and basocellular cancer 0.1% and 0.5% respectively). <h3>Conclusions</h3> Non-melanoma was the most common skin cancer observed in our SLE cohort. Its prevalence appeared to be higher than that reported in the general poopulation. SLE patients with melanoma showed a higher frequency of cutaneous lupus history compared with other SLE patients. <h3>References</h3> Cao L et al PLoS One 2015;10:1–21. Goobie GC et al. Current Opinion Rheumatology 2015;27:454–60. <h3>Disclosure of Interest</h3> None declared
Outcomes with Extracorporeal Photopheresis in the Management of Chronic Gvhd: A Multi-Centre Experience
Authors: David Routledge, John Murray, Fiona Dignan, Amanda Calderwood, Adrian Bloor, Eleni Tholouli, Therese Callaghan, Muhammad Ameer Saif, Michael Dennis, James Cavet, Samar Kulkarni
Journal: Blood (2016)
FRI0379 Prevalence of FAM111 B gene mutations in systemic sclerosis
Authors: A Gcelu, G Deshpande, AA Kalla, M Tikly, B Mayosi, B Hodkinson
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Systemic sclerosis (SSc) is a prototypic systemic fibrotic disease with unclearly characterized genetic basis. Implicated genes have been associated with autoimmune dysregulation with relatively few variants associated with fibrosis [1]. We have discovered that mutations in <i>FAM111B</i> gene cause hereditary fibrosing poikiloderma with tendon contractures, myopathy, and pulmonary fibrosis (POIKTMP)[2], a multisystem fibrotic condition with clinical aspects of SSc [3]. This observation has established <i>FAM111B</i> as a candidate gene for SSc. <h3>Objectives</h3> The objective is to investigate whether <i>FAM111B</i> gene mutations are present in SSc patients and further explore relationships between <i>FAM111B</i> mutations and clinical expression of SSc. <h3>Methods</h3> Patients with a definite diagnosis of SSc attending the Rheumatology outpatient departments at Groote Schuur Hospital, Cape Town, and Chris Hani Baragwanath Hospital, Johannesburg, were enrolled into the study. Physical examination assessing the extent of disease was done in all patients and the modified Rodnan skin score (mRSS) was used to determine the extent of the skin involvement. Blood samples were collected for DNA extraction and mutation screening using the high-resolution melt technique. Samples with abnormal electropherograms were selected for Sanger sequencing to identify mutations. Public databases were used to verify the frequency of variants in <i>FAM111B</i>. <h3>Results</h3> 131 patients were genotyped, 13 men and 118 women, with a mean age of 26.6 years and mean age of symptom onset at 25.3 years. The majority of patients were black (59.5%). 72% of patients had diffuse systemic sclerosis (DSSc) with a median mRSS of 11. Genetic analysis revealed seven rare genetic variants (C832G&gt;A; C855G&gt;T; C917A&gt;G; C937G&gt;A; C988C&gt;T; C995A&gt;C and C1006G&gt;C) in eight patients (five patients from Johannesburg and three patients from Cape Town) [table 1]. These variants were missense mutations of unknown significance with a minor allele frequency &lt;0.01. No <i>FAM111B</i> mutations that cause POIKMT were found in patients with SSc. <h3>Conclusions</h3> Rare genetic variants of unknown significance (GVUS) in <i>FAM111B</i> gene were found in patients with SSc. It is possible that the GVUS may modify the function of <i>FAM111B</i>, and influence the pathogenesis of SSc or are rare polymorphisms with no functional impact. <h3>References</h3> Romano, E., et al., The genetics of systemic sclerosis: an update. Clin Exp Rheumatol, 2011. 29(2 Suppl 65): p. S75–86. Mercier, S., et al., Mutations in FAM111B cause hereditary fibrosing poikiloderma with tendon contracture, myopathy, and pulmonary fibrosis. Am J Hum Genet, 2013. 93(6): p. 1100–7. Khumalo, N.P., et al., Poikiloderma, tendon contracture and pulmonary fibrosis: a new autosomal dominant syndrome? Br J Dermatol, 2006. 155(5): p. 1057–61. <h3>Disclosure of Interest</h3> None declared
SAT0571 Performing septic arthritis diagnosis in scenarios where synovial fluid is not available: multivariate logistic regression analysis
Authors: CA Guillen-Astete, GA Gabilondo-Alvarez
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> In order to establish the diagnosis of septic arthritis (SA) it is necessary to demonstrate the presence of bacteria into the synovial fluid. However, clinics should act according to its suspicious when the differential diagnosis included this possibility even when the microbiologic study of the synovial fluid in unavailable by any cause (small joints, lack of training or logistic deficiencies). <h3>Objectives</h3> The purpose of our study is to determine the relative weight of other clinical or analytical variables that should be useful in these scenarios. <h3>Methods</h3> A retrospective multivariate logistic regression analysis about the registries of monoarthritis assessed in our unit between 2013 and 2016. There were included only registries with cases of synovial joints with all parameters of interest available. The binary response variable was the microbiological demonstration of septic arthritis (culture/Gram stain of synovial fluid or tissue). Explanatory variables were age (stratified in &lt;30, 30–39, 40–49, 50–59, 60–69 and &gt;70 years old), gender, temperature above of 37.9°C, recount of neutrophils in peripheral blood sample, measure of procalcitonine (PCT), and measure of C reactive protein (CRP). Synovial fluid study, although was available in almost all cases was deliberately omitted for purpose of this study. The logistic regression analysis used the forward model strategy. <h3>Results</h3> There were included 449 registries. One hundred an sisteen of them were SA. The fixed model showed a Chi-square=226.64 with 5 degrees of freedom and a P&lt;0.0001. Explanatory variable gender was excluded from the forward model strategy due to its lack of impact on the binary response variable. The Odds Ratio for PCR, PCT &gt;1.3 ng/dL, age, neutrofils recount and body temperature were 1.0175, 8.1588, 0.5135, 1.0001 and 3.4147, respectively. The model showed a sensibility of 68.1%, specificity of 94.8%, PPV of 82.2% and NPV of 89.5%. The following table shows the full results of the logistic regression analysis: Standard error, Wald index, p value and R coefficients. <h3>Conclusions</h3> Previous studies have demonstrated the usefulness of PCT measure for the diagnosis of SA however all of them have been based on joints which synovial fluid is quite easy to obtain for further analysis. Present study allows laying the ground for creation of future diagnostic models based on five clinical variables that could be useful on scenarios where the assessment by joint puncture is not available. <h3>Disclosure of Interest</h3> None declared
FRI0029 The oxygen sensor phd1 is an indispensable regulator of arthritis development
Authors: K De Wilde, D Gaublomme, J Coudenys, F Windels, S Van Welden, A De Muynck, D Elewaut
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Oxygen supply is a fundamental requirement for all living tissues. Some tissues such as articular joints are characterized by a physiological state of hypoxia. Interestingly, under conditions of inflammation such as in arthritic disease, this level of hypoxia is even further enhanced. However, the functional significance of these observations and the molecular mechanisms involved remain poorly characterized to date. Our goal was therefore to examine the role of 3 known oxygen sensors, prolyl hydroxylase domain (PHD) proteins: PHD1, PHD2 and PHD3. They are enzymes whose function is essentially controlled by oxygen. Their expression pattern varies between either of them and all of them have been ascribed specific roles in a myriad of biological processes. [1] <h3>Objectives</h3> Our goal was to examine the role of oxygen sensors PHD1, PHD2 and PHD3 in preclinical models of rheumatoid arthritis, and to delineate the cellular source involved. <h3>Methods</h3> We subjected the collagen antibody induced arthritis (CAIA) model (resembling rheumatoid arthritis) to hypoxic (10% O<sub>2</sub>) and normoxic conditions (21% O<sub>2</sub>), respectively. Furthermore, the CAIA-model was induced in mice with germline deficiency of the specific PHD9s and in mice with a myeloid cell-specific PHD1 deficiency versus controls. Arthritis development was assessed by clinical scoring of paw swelling, histopathology of knee joints and μCT. <h3>Results</h3> Mice kept in hypoxic conditions during CAIA experiments showed markedly less arthritis (both by clinical and histopathological assessment) compared to mice in normoxic conditions. Furthermore, we demonstrated that PHD1 knock-out (KO) mice had significantly less joint inflammation compared to wildtype mice. PHD1 KO mice were also protected against inflammation induced bone loss as evidenced by μCT. By contrast, no differences were found between PHD2 heterozygous (PHD2 KO mice are not viable) or PHD3 KO mice and littermate controls. Because myeloid cells are considered critical effector cells upon passive transfer of arthritogenic antibodies in the CAIA model we also generated myeloid cell specific ko mice (PHD1<sup>myelKO</sup>). Of interest, PHD1<sup>myelKO</sup> mice developed less arthritis compared to wildtype mice and were protected against inflammation induced bone loss. <h3>Conclusions</h3> Our data are consistent with a new paradigm that the oxygen sensor PHD1 is a critical regulator of myeloid cell function in arthritic disease. Overall, the data suggest that PHD1 is a potential target in the treatment of arthritis. <h3>References</h3> Fong G-H, Takeda K. Role and regulation of prolyl hydroxylase domain proteins. Cell Death Differ 2008;15:635–41. doi:10.1038/cdd.2008.10. <h3>Disclosure of Interest</h3> None declared
AB0216 Effects of anti-citrullinated protein antibodies on systemic bone mass in rheumatoid arthritis patients
Authors: G Orsolini, C Caimmi, O Viapiana, L Idolazzi, E Fracassi, D Gatti, G Adami, M Rossini
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Bone loss in rheumatoid arthritis (RA) is a key feature both local and systemic. Anti-citrullinated protein antibodies (ACPA) have recently been found to directly induce differentiation and activation of osteoclasts and therefore contribute to periarticular bone loss. <h3>Objectives</h3> The aim of this study was to analyze the effect of ACPA on systemic bone mineral density (BMD) in patients with established RA. <h3>Methods</h3> This is a cross-sectional study with a single-center RA population. BMD was measured with Dual X-ray absorptiometry at lumbar and femoral sites. ACPA were measured by EIA. Multivariate analysis was performed adjusting for the main confounding variables. <h3>Results</h3> One hundred twenty-seven RA patients were enrolled. In univariate analysis ACPA-positive patients showed lower BMD Z-score (SD below the age- and gendermatched mean reference value) at femoral sites (p&lt;0.01). A negative correlation between ACPA titer and BMD Z-score at all sites was observed (p&lt;0.01). The multivariate analysis adjusted for the main confounding variables confirmed the negative effect of ACPA at femoral sites (p&lt;0.05), but not at lumbar spine BMD. No significant effect of rheumatoid factor has been observed. <h3>Conclusions</h3> ACPA have a negative titer-dependent effect on BMD at femoral sites, mainly constituted by cortical bone. ACPA-positive patients, especially if at high titer, should undergo bone investigations and be treated with bone protecting agents. Disease-modifying anti-rheumatic drugs lowering ACPA titer might have positive effects on systemic bone mass. <h3>Disclosure of Interest</h3> None declared
SP0124 Health economics and health equity: two complementary disciplines
Authors: B Fautrel
Journal: Annals of the Rheumatic Diseases (2017)

Health equity in the one hand refers to the absence of systematic disparities in health between different social groups in a given Society, a province, a country or a group of country. Health inequity thus corresponds to a situation in which health services are not similarly available to all people with the same health conditions and health needs, due to individual personal or socioeconomic characteristics. Health economics in the other hand focuses on how to allocate health budgets in order to maximize the general health of the population as a whole. With regards to this, no specific attention is dedicated to socially disadvantaged subgroups. In addition, the most visible action in the field of health economics was the valorization of therapeutic innovation, i.e., the determination of its price not on production costs but on the value associated with this innovation. Economic evaluation – i.e., determination of incremental cost-effectiveness ration – has lead during the last 20 years to substantial financial pressure on health care systems with dramatic increase in health expenditures mainly due to the costs of therapeutic innovation. Several studies have shown that such a process may increase health inequities within a country or a group of countries if specific actions are not taken to maintain or improve treatment availability and access to care to all the population members whatever their social, educational and economic characteristics. <h3>Disclosure of Interest</h3> None declared
SP0049 Dna aggregates as alarmins
Authors: D Pisetsky
Journal: Annals of the Rheumatic Diseases (2017)

DNA is a large polymeric molecule that displays powerful immunological activities and operates in the context of multi-component aggregates to alarm the immune system and stimulate innate immunity. Although DNA has important roles in normal host defense, DNA can serve as an autoantigen and autoimmunogen by itself or in association with other immunologically active nuclear molecules. In the setting of systemic lupus erythematosus (SLE), DNA is a key target antigen; while antibodies to pure DNA double stranded DNA serve as important biomarkers, the relevant antigenic form of DNA during disease is the nucleosome in which DNA is bound to histones. Furthermore, nucleosomes can be components of microparticles which are small membrane-bound structures that are released from dead and dying cells. MPs can stimulate immune responses and serve as a nidus for immune complex formation. In normal immunity, DNA can interact with nucleic acid sensors in the cytoplasm of cells to stimulate responses including production of type 1 interferon. These sensors respond to DNA from intracellular organisms such as bacteria and viruses although damaged DNA and DNA from mitochondria can also interact with these receptors. While these sensors are intracellular, they can interact with extracellular DNA that is introduced or transfected into the cell; this translocation event occurs with DNA bound with other molecules. In another facet of host defense, DNA can be released from neutrophils during a process termed NETosis. A NET or neutrophil extracellular trap is a mesh-like structure comprised of DNA as well as granule proteins that have antibacterial activity. NETs can trap and kill bacteria. Thus, in its diverse immunological roles, DNA interacts with other molecules to form aggregates or sub-cellular structures that alarm the immune system, promote host defense or drive critical events in autoimmunity. <h3>Disclosure of Interest</h3> None declared
Omission of Data and Errors in Meta-analysis
Authors: Hon-Yen Wu
Journal: JAMA Internal Medicine (2017)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Internal Medicine journal