An one-stop career platform detailing Schools & Universities offering English language, Bachelor, Master and PhD programs with course fee, living cost, scholarships, visa details, etc.
---------------------------
Cyprus College
cycollege.ac.cy
The college was founded in 1961 with the purpose to provide a well rounded education of high calibre where students can acquire the necessary academic knowledge.
---------------------------
Wroclaw University
international.uni.wroc.pl
Founded in 1702 by Leopold I Habsburg. Since the beginning of 20th century the university has produced 9 Nobel Prize winners.
---------------------------
Volyn University
vdu.edu.ua
The history dates back to 1940. At present, the university includes 4 institutes, 14 faculties and 73 departments.
---------------------------
Berkeley College
berkeleycollege.edu
Through the power of internet, Berkeley college online brings the classroom to you anywhere in the world with the same high level of support as On-Campus classes.
---------------------------
AIS
ais.ac.nz
New Zealand's largest international degree provider. The programmes are focused on the global marketplace.
---------------------------
WORLD UNIVERSITY DIRECTORY
Medical Education Annals of the Rheumatic Diseases current issue
<p>Morand EF, Abreu G, Furie RA, <I>et al</I>. Lupus low disease activity state attainment in the phase 3 TULIP trials of anifrolumab in active systemic lupus erythematosus. <I>Annals of the Rheumatic Diseases</I> 2023;82:639-645.</p> <p>This note aims to correct an error in the DORIS (Definition of Remission in SLE) data in the Morand E, <I>et al</I>. (2023) article. In the version of this article initially published, analyses of DORIS remission excluded all laboratory parameters in the calculation of clinical SLEDAI-2K (cSLEDAI-2K), consistent with the cSLEDAI-2K definition in the TULIP protocols. The updated analysis aligns with the published DORIS remission definition by excluding only the serologic laboratory parameters from cSLEDAI-2K. These updates do not change the conclusions of the findings and this correction aligns the analysis with the validated DORIS remission definition that is now promulgated in the 2023 EULAR SLE treatment guidelines. Changes are summarised below:</p> <p>The corrected definition of...
<p>Ankylosing spondylitis (AS) is the historic term used for decades for the HLA-B27-associated inflammatory disease affecting mainly the sacroiliac joints (SIJ) and spine. Classification criteria for AS have radiographic sacroiliitis as a dominant characteristic. However, with the availability of MRI of SIJ, it could be demonstrated that the disease starts long before definite SIJ changes become visible on radiographs. The Assessment of SpondyloArthritis international Society, representing a worldwide group of experts reached consensus on changes in the nomenclature pertaining to axial spondyloarthritis (axSpA), such as the terminology of diagnosis and of assessment of disease activity tools. These are important changes in the field, as experts in axSpA are now in agreement that the term axSpA is the overall term for the disease. A further differentiation, of which <I>radiographic</I> versus <I>non-radiographic</I> is only one aspect, may be relevant for research purposes. Another important decision was that the terms AS and radiographic axSpA (r-axSpA) can be used interchangeably, but that the preferred term is r-axSpA. Based on the decision that axSpA is the correct terminology, a proposal was made to officially change the meaning of the ASDAS acronym to ‘Axial Spondyloarthritis Disease Activity Score’. In addition, for simplification it was proposed that the term ASDAS (instead of ASDAS-CRP) should be preferred and applied to the ASDAS calculated with C reactive protein (CRP). It is hoped that these changes will be used consequently for education, in textbooks, manuscripts and presentations.</p>
<p>A hallmark of rheumatoid arthritis (RA) is the increased levels of autoantibodies preceding the onset and contributing to the classification of the disease. These autoantibodies, mainly anti-citrullinated protein antibody (ACPA) and rheumatoid factor, have been assumed to be pathogenic and many attempts have been made to link them to the development of bone erosion, pain and arthritis. We and others have recently discovered that most cloned ACPA protect against experimental arthritis in the mouse. In addition, we have identified suppressor B cells in healthy individuals, selected in response to collagen type II, and these cells decrease in numbers in RA. These findings provide a new angle on how to explain the development of RA and maybe also other complex autoimmune diseases preceded by an increased autoimmune response.</p>
<sec><st>Objectives</st>
<p>We aimed to cluster patients with rheumatoid arthritis (RA) based on comorbidities and then examine the association between these clusters and RA disease activity and mortality.</p>
</sec>
<sec><st>Methods</st>
<p>In this population-based study, residents of an eight-county region with prevalent RA on 1 January 2015 were identified. Patients were followed for vital status until death, last contact or 31 December 2021. Diagnostic codes for 5 years before the prevalence date were used to define 55 comorbidities. Latent class analysis was used to cluster patients based on comorbidity patterns. Standardised mortality ratios were used to assess mortality.</p>
</sec>
<sec><st>Results</st>
<p>A total of 1643 patients with prevalent RA (72% female; 94% white; median age 64 years, median RA duration 7 years) were studied. Four clusters were identified. Cluster 1 (n=686) included patients with few comorbidities, and cluster 4 (n=134) included older patients with 10 or more comorbidities. Cluster 2 (n=200) included patients with five or more comorbidities and high prevalences of depression and obesity, while cluster 3 (n=623) included the remainder. RA disease activity and survival differed across the clusters, with cluster 1 demonstrating more remission and mortality comparable to the general population.</p>
</sec>
<sec><st>Conclusions</st>
<p>More than 40% of patients with prevalent RA did not experience worse mortality than their peers without RA. The cluster with the worst prognosis (<10% of patients with prevalent RA) was older, had more comorbidities and had less disease-modifying antirheumatic drug and biological use compared with the other clusters. Comorbidity patterns may hold the key to moving beyond a one-size-fits-all perspective of RA prognosis.</p>
</sec>
<sec><st>Objective</st>
<p>Erythropoietin (EPO) known as an erythrocyte-stimulating factor is increased in patients with rheumatoid arthritis (RA). Nevertheless, the function of EPO in the process of RA and relative mechanism needs to be further clarified.</p>
</sec>
<sec><st>Methods</st>
<p>The level of EPO in serum and synovial fluid from patients with RA and healthy controls was determined by . Collagen-induced arthritis (CIA) mice were constructed to confirm the role of EPO on RA pathogenesis. Differentially expressed genes (DEGs) of EPO-treated fibroblast-like synoviocyte (FLS) were screened by transcriptome sequencing. The transcription factor of neuraminidase 3 (NEU3) of DEGs was verified by double luciferase reporting experiment, DNA pulldown, electrophoretic mobility shift assay and chromatin immunoprecipitation-quantitative PCR (qPCR) assay.</p>
</sec>
<sec><st>Results</st>
<p>The overexpression of EPO was confirmed in patients with RA, which was positively associated with Disease Activity Score 28-joint count. Additionally, EPO intervention could significantly aggravate the joint destruction in CIA models. The upregulation of NEU3 was screened and verified by transcriptome sequencing and qPCR in EPO-treated FLS, and signal transducer and activator of transcription 5 was screened and verified to be the specific transcription factor of NEU3. EPO upregulates NEU3 expression via activating the Janus kinase 2 (JAK2)-STAT5 signalling pathway through its receptor EPOR, thereby to promote the desialylation through enhancing the migration and invasion ability of FLS, which is verified by JAK2 inhibitor and NEU3 inhibitor.</p>
</sec>
<sec><st>Conclusion</st>
<p>EPO, as a proinflammatory factor, accelerates the process of RA through transcriptional upregulation of the expression of NEU3 by JAK2/STAT5 pathway.</p>
</sec>
<sec><st>Objectives</st>
<p>B10 and B10pro cells suppress immune responses via secreting interleukin (IL)-10. However, their regulators and underlying mechanisms, especially in human autoimmune diseases, are elusive. This study aimed to address these questions in rheumatoid arthritis (RA), one of the most common highly disabling autoimmune diseases.</p>
</sec>
<sec><st>Methods</st>
<p>The frequencies and functions of B10 and B10pro cells in healthy individuals and patients with RA were first analysed. The effects of proinflammatory cytokines, particularly tumour necrosis factor (TNF)-α on the quantity, stability and pathogenic phenotype of these cells, were then assessed in patients with RA before and after anti-TNF therapy. The underlying mechanisms were further investigated by scRNA-seq database reanalysis, transcriptome sequencing, TNF-α<sup>–/–</sup> and B cell-specific SHIP-1<sup>–/–</sup> mouse disease model studies.</p>
</sec>
<sec><st>Results</st>
<p>TNF-α was a key determinant for B10 cells. TNF-α elicited the proinflammatory feature of B10 and B10pro cells by downregulating IL-10, and upregulating interferon- and IL-17A. In patients with RA, B10 and B10pro cells were impaired with exacerbated proinflammatory phenotype, while anti-TNF therapy potently restored their frequencies and immunosuppressive functions, consistent with the increased B10 cells in TNF-α<sup>–/–</sup> mice. Mechanistically, TNF-α diminished B10 and B10pro cells by inhibiting their glycolysis and proliferation. TNF-α also regulated the phosphatidylinositol phosphate signalling of B10 and B10pro cells and dampened the expression of SHIP-1, a dominant phosphatidylinositol phosphatase regulator of these cells.</p>
</sec>
<sec><st>Conclusions</st>
<p>TNF-α provoked the proinflammatory phenotype of B10 and B10pro cells by disturbing SHIP-1 in RA, contributing to the disease development. Reinstating the immunosuppressive property of B10 and B10pro cells might represent novel therapeutic approaches for RA.</p>
</sec>
<sec><st>Objectives</st>
<p>To investigate the prevalence of axial spondyloarthritis (axSpA) in patients with chronic back pain (CBP) of less than 2 years (2y) duration referred to the rheumatologist, the development of diagnosis over time, and patient characteristics of those developing <I>definite (d-)axSpA</I> over 2y.</p>
</sec>
<sec><st>Methods</st>
<p>We analysed the 2y data from SPondyloArthritis Caught Early, a European cohort of patients (<45 years) with CBP (≥3 months, ≤2y) of unknown origin. The diagnostic workup comprised evaluation of clinical SpA features, acute phase reactants, HLA-B27, radiographs and MRI (sacroiliac joints and spine), with repeated assessments. At each visit (baseline, 3 months, 1y and 2y), rheumatologists reported a diagnosis of <I>axSpA</I> or <I>non-axSpA</I> with level of confidence (LoC; 0-<I>not confident at all</I> to 10-<I>very confident</I>). Main outcome: axSpA diagnosis with LoC≥7 (<I>d-axSpA</I>) at 2y.</p>
</sec>
<sec><st>Results</st>
<p>In 552 patients with CBP, <I>d-axSpA</I> was diagnosed in 175 (32%) at baseline and 165 (30%) at 2y. Baseline diagnosis remained rather stable: at 2y, baseline <I>d-axSpA</I> was revised in 5% of patients, while 8% ‘gained’ <I>d-axSpA</I>. Diagnostic uncertainty persisted in 30%. HLA-B27+ and baseline sacroiliitis imaging discriminated best 2y-<I>d-axSpA</I> versus 2y-<I>d-non-axSpA</I> patients. Good response to non-steroidal anti-inflammatory drugs and MRI-sacroiliitis most frequently developed over follow-up in patients with a new <I>d-axSpA</I> diagnosis. Of the patients who developed MRI-sacroiliitis, 7/8 were HLA-B27+ and 5/8 male.</p>
</sec>
<sec><st>Conclusion</st>
<p>A diagnosis of <I>d-axSpA</I> can be reliably made in nearly one-third of patients with CBP referred to the rheumatologist, but diagnostic uncertainty may persist in 5%–30% after 2y. Repeated assessments yield is modest, but repeating MRI may be worthwhile in male HLA-B27+ patients.</p>
</sec>
<sec><st>Objectives</st>
<p>The study aimed to evaluate the effect of adding a non-steroidal anti-inflammatory drug (NSAID), celecoxib (CEL), to a tumour necrosis factor inhibitor (TNFi), golimumab (GOL), compared with TNFi monotherapy on radiographic spinal progression in patients with radiographic axial spondyloarthritis (r-axSpA) over 2 years.</p>
</sec>
<sec><st>Methods</st>
<p>R-axSpA patients, having risk factors for radiographic progression (high disease activity plus C reactive protein >5 mg/L and/or ≥1 syndesmophyte(s)), underwent a 12-week run-in phase with GOL 50 mg every 4 weeks. In the core phase (96 weeks), only patients with a good clinical response at week 12 were randomised (1:1) to GOL+CEL 200 mg two times per day (combination therapy) or GOL monotherapy. The primary endpoint was radiographic progression assessed by modified Stoke Ankylosing Spondylitis Spinal Score (mSASSS) change at week 108 in the intent-to-treat population.</p>
</sec>
<sec><st>Results</st>
<p>A total of 128 patients were enrolled in the run-in phase; and 109 patients were randomised at week 12 to monotherapy (n=55) or combination therapy (n=54). At week 108, 97 (52 vs 45) patients completed the study. The change in mSASSS at week 108 was 1.7 (95% CI 0.8 to 2.6) in the monotherapy vs 1.1 (95% CI 0.4 to 1.8) in the combination therapy groups (p=0.79). New syndesmophytes occurred in 25% of patients in the monotherapy vs 11% of patients in the combination therapy groups (p=0.12). During the study, no significant differences in adverse events and serious adverse events were observed between the groups.</p>
</sec>
<sec><st>Conclusions</st>
<p>Combination therapy with GOL+CEL did not demonstrate statistically significant superiority over GOL monotherapy in retarding radiographic spinal progression over 2 years in r-axSpA.</p>
</sec>
<sec><st>Objectives</st>
<p>The current work aimed to provide a comprehensive single-cell landscape of lupus nephritis (LN) kidneys, including immune and non-immune cells, identify disease-associated cell populations and unravel their participation within the kidney microenvironment.</p>
</sec>
<sec><st>Methods</st>
<p>Single-cell RNA and T cell receptor sequencing were performed on renal biopsy tissues from 40 patients with LN and 6 healthy donors as controls. Matched peripheral blood samples from seven LN patients were also sequenced. Multiplex immunohistochemical analysis was performed on an independent cohort of 60 patients and validated using flow cytometric characterisation of human kidney tissues and in vitro assays.</p>
</sec>
<sec><st>Results</st>
<p>We uncovered a notable enrichment of CD163<sup>+</sup> dendritic cells (DC3s) in LN kidneys, which exhibited a positive correlation with the severity of LN. In contrast to their counterparts in blood, DC3s in LN kidney displayed activated and highly proinflammatory phenotype. DC3s showed strong interactions with CD4<sup>+</sup> T cells, contributing to intrarenal T cell clonal expansion, activation of CD4<sup>+</sup> effector T cell and polarisation towards Th1/Th17. Injured proximal tubular epithelial cells (iPTECs) may orchestrate DC3 activation, adhesion and recruitment within the LN kidneys. In cultures, blood DC3s treated with iPTECs acquired distinct capabilities to polarise Th1/Th17 cells. Remarkably, the enumeration of kidney DC3s might be a potential biomarker for induction treatment response in LN patients.</p>
</sec>
<sec><st>Conclusion</st>
<p>The intricate interplay involving DC3s, T cells and tubular epithelial cells within kidneys may substantially contribute to LN pathogenesis. The enumeration of renal DC3 holds potential as a valuable stratification feature for guiding LN patient treatment decisions in clinical practice.</p>
</sec>
<sec><st>Objectives</st>
<p>Obstetric antiphospholipid syndrome (OAPS) is an autoimmune disease characterised by the presence of antiphospholipid antibodies in circulation and pathological pregnancy. However, the pathogenesis of OAPS remains unknown. We aimed to reveal cellular compositions and molecular features of decidual cells involved in the development of OAPS using single-cell RNA sequencing (scRNA-seq).</p>
</sec>
<sec><st>Methods</st>
<p>We performed unbiased scRNA-seq analysis on the first-trimester decidua from five OAPS patients and five healthy controls (HCs), followed by validations with flow cytometry, immunohistochemical staining and immunofluorescence in a larger cohort. Serum chemokines and cytokines were measured by using ELISA.</p>
</sec>
<sec><st>Results</st>
<p>A higher ratio of macrophages but a lower ratio of decidual natural killer (dNK) cells was found in decidua from OAPS compared with HCs. Vascular endothelial cells shrinked in OAPS decidua while having upregulated chemokine expression and conspicuous responses to IFN- and TNF-α. Macrophages in OAPS had stronger phagocytosis function, complement activation signals and relied more on glycolysis. dNK cells were more activated in OAPS and had enhanced cytotoxicity and IFN- production. Downregulation of granules in OAPS dNK cells could be associated with suppressed glycolysis. Moreover, stromal cells had a prosenescent state with weakened immune surveillance for senescent cells in OAPS. In addition, the cellular interactions between decidual immune cells and those of immune cells with non-immune cells under disease state were altered, especially through chemokines, IFN- and TNF-α.</p>
</sec>
<sec><st>Conclusion</st>
<p>This study provided a comprehensive decidual cell landscape and identified aberrant decidual microenvironment in OAPS, providing some potential therapeutic targets for this disease.</p>
</sec>
<sec><st>Objectives</st>
<p>Based on genetic associations, McGonagle and McDermott suggested a classification of autoimmune and autoinflammatory diseases as a continuum ranging from purely autoimmune to purely autoinflammatory diseases and comprising diseases with both components. We used deep immunophenotyping to identify immune cell populations and molecular targets characterising this continuum.</p>
</sec>
<sec><st>Methods</st>
<p>We collected blood from 443 patients with one of 15 autoimmune or autoinflammatory diseases and 71 healthy volunteers. Deep phenotyping was performed using 13 flow cytometry panels characterising over 600 innate and adaptive cell populations. Unsupervised and supervised analyses were conducted to identify disease clusters with their common and specific cell parameters.</p>
</sec>
<sec><st>Results</st>
<p>Unsupervised clustering categorised these diseases into five clusters. Principal component analysis deconvoluted this clustering into two immunological axes. The first axis was driven by the ratio of LAG3+ to ICOS+ in regulatory T lymphocytes (Tregs), and segregated diseases based on their inflammation levels. The second axis was driven by activated Tregs and type 3 innate lymphoid cells (ILC3s), and segregated diseases based on their types of affected tissues. We identified a signature of 23 cell populations that accurately characterised the five disease clusters.</p>
</sec>
<sec><st>Conclusions</st>
<p>We have refined the monodimensional continuum of autoimmune and autoinflammatory diseases as a continuum characterised by both disease inflammation levels and targeted tissues. Such classification should be helpful for defining therapies. Our results call for further investigations into the role of the LAG3+/ICOS+ balance in Tregs and the contribution of ILC3s in autoimmune and autoinflammatory diseases.</p>
</sec>
<sec><st>Trial registration number</st>
<p> <A HREF="NCT02466217">NCT02466217</A>.</p>
</sec>
<sec><st>Objectives</st>
<p>IgG4-related disease (IgG4-RD) is an immune-mediated, fibroinflammatory disease. Induction treatment with glucocorticoid (GC) is usually effective, but its tendency of relapse makes the strategy for maintenance treatment a challenge. The WInS IgG4-RD (withdraw immunosuppressants (IMs) and steroid in stable IgG4-RD) trial tested whether discontinuation of GC and IM was feasible in stable IgG4-RD.</p>
</sec>
<sec><st>Methods</st>
<p>The WInS IgG4-RD trial was a multicentre, open-label, randomised controlled trial. Patients with IgG4-RD receiving GC+IM as maintenance treatment with clinically quiescent disease for at least 12 months were randomised (1:1:1) into three groups: group 1: withdraw GC+IM; group 2: withdraw GC but maintain IM; group 3: maintain GC+IM. The primary outcome was the relapse rate of disease within 18 months. The secondary outcomes included the changes of IgG4-RD Responder Index (RI), Physician’s Global Assessment (PGA), serum IgG4 and IgG, as well as adverse events.</p>
</sec>
<sec><st>Results</st>
<p>One hundred and forty-six patients were randomised, with 48 patients in group 1, 49 patients in group 2 and group 3, respectively. Within the 18-month follow-up period, disease relapse occurred in 25 out of 48 (52.1%) patients in group 1 vs 7 out of 49 (14.2%) in group 2 and 6 out of 49 (12.2%) in group 3 (p<0.001). The changes in RI and PGA were significantly higher in group 1 than in group 2 (p<0.001) or group 3 (p<0.001).</p>
</sec>
<sec><st>Conclusions</st>
<p>The maintenance of IMs, with or without low-dose GC, was found to be superior to withdraw GC+IM in preventing relapse for long-time stable IgG4-RD.</p>
</sec>
<sec><st>Trial registration number</st>
<p> <A HREF="NCT04124861">NCT04124861</A>.</p>
</sec>
<sec><st>Objective</st>
<p>Early diagnosis of knee osteoarthritis (KOA) in asymptomatic stages is essential for the timely management of patients using preventative strategies. We develop and validate a prognostic model useful for predicting the incidence of radiographic KOA (rKOA) in non-radiographic osteoarthritic subjects and stratify individuals at high risk of developing the disease.</p>
</sec>
<sec><st>Methods</st>
<p>Subjects without radiographic signs of KOA according to the Kellgren and Lawrence (KL) classification scale (KL=0 in both knees) were enrolled in the OA initiative (OAI) cohort and the Prospective Cohort of A Coruña (PROCOAC). Prognostic models were developed to predict rKOA incidence during a 96-month follow-up period among OAI participants based on clinical variables and serum levels of the candidate protein biomarkers APOA1, APOA4, ZA2G and A2AP. The predictive capability of the biomarkers was assessed based on area under the curve (AUC), and internal validation was performed to correct for overfitting. A nomogram was plotted based on the regression parameters. Model performance was externally validated in the PROCOAC.</p>
</sec>
<sec><st>Results</st>
<p>282 participants from the OAI were included in the development dataset. The model built with demographic, anthropometric and clinical data (age, sex, body mass index and WOMAC pain score) showed an AUC=0.702 for predicting rKOA incidence during the follow-up. The inclusion of ZA2G, A2AP and APOA1 data significantly improved the model’s sensitivity and predictive performance (AUC=0.831). The simplest model, including only clinical covariates and ZA2G and A2AP serum levels, achieved an AUC=0.826. Both models were internally cross-validated. Predictive performance was externally validated in an independent dataset of 100 individuals from the PROCOAC (AUC=0.713).</p>
</sec>
<sec><st>Conclusion</st>
<p>A novel prognostic model based on common clinical variables and protein biomarkers was developed and externally validated to predict rKOA incidence over a 96-month period in individuals without any radiographic signs of disease. The resulting nomogram is a useful tool for stratifying high-risk populations and could potentially lead to personalised medicine strategies for treating OA.</p>
</sec>
<sec><st>Objectives</st>
<p>To investigate the associations of residential greenness with bone mineral density and incident osteoporosis, and further evaluate the potential modifying effect of genetic susceptibility.</p>
</sec>
<sec><st>Methods</st>
<p>We used the Normalised Difference Vegetation Index (NDVI) at various buffer distances, including 300 m (NDVI<SUB>300m</SUB>), 500 m (NDVI<SUB>500m</SUB>), 1000 m (NDVI<SUB>1000m</SUB>) and 1500 m (NDVI<SUB>1500m</SUB>), to serve as indicators of greenness. We fitted linear regression, logistic regression and Cox proportional hazard models to assess the associations of residential greenness with estimated bone mineral density (eBMD), prevalent osteoporosis and incident osteoporosis, respectively. With the Polygenic Risk Score (PRS) for osteoporosis, we further assessed the joint effects of genetic risk and greenness on the risk of osteoporosis. We conducted causal mediation analyses to explore potential mediators.</p>
</sec>
<sec><st>Results</st>
<p>Each IQR increase in NDVI<SUB>300m</SUB> was associated with 0.0007 (95% CI 0.0002 to 0.0013) increase in eBMD, 6% lower risk of prevalent osteoporosis (OR 0.94; 95% CI 0.92 to 0.97) and 5% lower risk of incident osteoporosis (HR 0.95; 95% CI 0.93 to 0.98). The joint effects of greenness and PRS on the risk of osteoporosis displayed a clear dose-response pattern. Compared with individuals exposed to low NDVI levels and high genetic risk, those exposed to high NDVI levels and low genetic risk had a 56% (95% CI 51% to 61%) lower risk of osteoporosis. The primary mediators in the association between greenness and incident osteoporosis were identified as PM<SUB>2.5</SUB> and NO<SUB>2</SUB>.</p>
</sec>
<sec><st>Conclusions</st>
<p>Residential greenness was associated with higher bone mineral density and decreased risk of incident osteoporosis.</p>
</sec>
<p>A 29-year-old woman presented to our rheumatology clinic with a 6-month history of cough, dysphonia, dyspnoea and weight loss. She also complained of a lump in her throat (globus pharyngeus), left otalgia and hearing loss. One month before evaluation, she started experiencing blood-tinged sputum and dyspnoea. On clinical examination, the patient had nasal discharge, crusting and congestion, laryngeal oedema, stridor, tympanic membrane retraction and external auditory canal ecchymosis.</p> <p>Laboratory findings showed anaemia (haemoglobin: 75.4 g/L, normal: 122.0–181.9), lymphocytosis 4.63<FONT FACE="arial,helvetica">x</FONT>10<sup>9</sup>/L (normal: 0.60<FONT FACE="arial,helvetica">x</FONT>10<sup>9</sup>–3.4<FONT FACE="arial,helvetica">x</FONT>10<sup>9</sup>/L), C reactive protein 13 mg/L and erythrocyte sedimentation rate 10 mm/hour. Serum creatinine level and urinalysis with urine sediment findings were normal.</p> <p>CT scan revealed sinonasal congestion, laryngeal oedema, pulmonary nodules and a symmetric 5 mm thickening of the aortic wall from the ascending to the descending aorta (<cross-ref type="fig" refid="F1">figure 1</cross-ref>). Bronchoscopy revealed ulcerated lesions in the trachea. Bacterial, fungal and mycobacterial cultures were negative. Reverse transcription PCR and interferon-gamma...
<p>New definitions for flares in rheumatoid arthritis (RA) based on the Simplified and Clinical Disease Activity Indices (SDAI, CDAI) have been recently introduced.<cross-ref type="bib" refid="R1">1</cross-ref> In this article, the authors defined flare as an absolute increase of 4.7 in SDAI and 4.5 in CDAI. Following this proposal we aimed at studying these cut-off values for absolute increases in SDAI and CDAI in diagnosing self-reported flares and treatment escalation in two separate real-world cohorts of patients with RA in France.</p> <p>The first cohort included 101 patients with established RA,<cross-ref type="bib" refid="R2">2</cross-ref> recruited between May 2016 and February 2018 and annually evaluated in day hospitalisation (<cross-ref type="tbl" refid="T1">table 1</cross-ref>). We collected data from their initial visit and their 12-month follow-up. The second cohort consisted of 272 patients with established RA in remission or low disease activity, defined by SDAI ≤11 and CDAI ≤10. Among these patients, 73 had a second visit with...
<p>The US Centers for Disease Control and Prevention (CDC) recommends three SARS-CoV-2 messenger ribonucleic acid (mRNA) vaccine doses, rather than two, to complete the initial vaccine series for immunosuppressed patients. However, they may remain at risk for breakthrough COVID-19 due to immunomodulators that blunt vaccine responses.<cross-ref type="bib" refid="R1">1</cross-ref> Identifying patients at highest risk for breakthrough COVID-19 can prioritise resources for prevention. Therefore, we investigated the risk of breakthrough COVID-19 among fully vaccinated patients with rheumatoid arthritis (RA) using disease-modifying antirheumatic drugs (DMARDs) and/or glucocorticoids, hypothesising that CD20 inhibitor (CD20i) users would have higher breakthrough COVID-19 risk than tumour necrosis factor inhibitor (TNFi) users.</p> <p>We performed a retrospective cohort study investigating immunomodulators and breakthrough COVID-19 risk among patients with RA who received three mRNA vaccines at Mass General Brigham, a multicentre healthcare system in Boston, Massachusetts, USA. A previously validated algorithm was used to identify patients with RA (postive predictive...
<p>Gender imbalance is a major source of inequity in the society. Inequality is an enduring topic also in medical research, as disparities in the participation of individuals based on their gender may potentially influence the research outcomes. Gender inequality often manifests as a lower representation of women as study authors or even their complete absence from research teams. Underlying causes may stem from differences in educational levels, gender-based discrimination and other factors.<cross-ref type="bib" refid="R1">1 2</cross-ref><cross-ref type="bib" refid="R2"></cross-ref> For example, in many countries, women still do the majority of unpaid domestic tasks such as childcare and housework.<cross-ref type="bib" refid="R3">3</cross-ref> Women with children also face particular barriers to actively participate in research.<cross-ref type="bib" refid="R3">3</cross-ref></p> <p>Clinical practice recommendation is instructive documents for guiding healthcare professionals in their practices, developed based on evidence derived from systematic reviews.<cross-ref type="bib" refid="R4">4</cross-ref> The assemble of a multidisciplinary and gender-balanced expert panel is a crucial step in...
Home
Contact Us
Back to "News Updates - Homepage"
