Academic literature on the topic 'Rheumatology and arthritis'

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Journal articles on the topic "Rheumatology and arthritis"

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Baillet, Athan, Candice Trocmé, Xavier Romand, Chuong M. V. Nguyen, Anais Courtier, Bertrand Toussaint, Philippe Gaudin, and Olivier Epaulard. "Calprotectin discriminates septic arthritis from pseudogout and rheumatoid arthritis." Rheumatology 58, no. 9 (March 28, 2019): 1644–48. http://dx.doi.org/10.1093/rheumatology/kez098.

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Abstract Objective We aimed to determine whether calprotectin and α-defensins could discriminate septic from other inflammatory arthritides. Methods Synovial fluids with a predominance of neutrophils from patients with septic arthritis, pseudogout and RA were prospectively collected. Neutrophil-related proteins calprotectin and human neutrophil α-defensins levels were assessed in synovial fluids. Demographic parameters and biomarkers with P-value ⩽0.05 for differentiating septic from non-septic arthritis were included in a multivariable model. Multivariable logistic regression with stepwise selection was performed to build the final combined model. Results A total of 74 patients were included: septic arthritis (n = 26), pseudogout (n = 28) and RA (n = 20). Patients with septic arthritis were more likely to be male and young, and to display higher synovial neutrophil count. Calprotectin was significantly increased in patients with septic arthritis. The multivariable model included calprotectin, synovial fluid neutrophil count and gender. Calprotectin was the only biomarker that discriminated septic arthritis from non-septic inflammatory arthritides, with 76% sensitivity, 94% specificity and a positive likelihood ratio = 12.2 at the threshold for calprotectin of 150 mg/l. Conclusion Synovial fluid calprotectin is a relevant biomarker to discriminate septic arthritis from other inflammatory arthritides. This biomarker should be tested in an independent cohort.
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ODEWUSI, OO, MJ ABDULMUMIN, and OO OLANIYAN. "AN ASSESSMENT OF AUTOIMMUNITY IN ARTHRITIS PATIENTS." International Journal of Medical Laboratory Research 07, no. 01 (2022): 53–61. http://dx.doi.org/10.35503/ijmlr.2022.7108.

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Objectives: The goal of this study is to estimate autoimmune biomarkers that characterize the development and severity of arthritis, but probably normalize following successful therapy. Materials and methods: In this study a total of 109 subjects were used out of which treated and untreated arthritics were 48 and 44 respectively, the remaining 17 were healthy individuals which were used as control. Samples were collected from patients attending Rheumatology and Orthopedic clinic of Federal Teaching Hospital Ido-ekiti, Ekiti State Nigeria. Antinuclear antibody was estimated using Enzyme Linked Immunosorbent Assay (ELISA) while Lupus Erythematosus cells were ascertained microscopically using Leishman staining technique. All parameters were assessed in treated and untreated arthritic patients relative to healthy subjects. Body mass index was also calculated. Statistical analysis was done using SPSS. Results: Body mass index and Antinuclear antibodies were significantly higher in treated and untreated arthritics compared to control (P<0.05). When treated and untreated arthritics were compared, Body mass index and Antinuclear antibody were found to be significantly higher in untreated arthritics (P<0.05). Antinuclear antibody and Age correlated directly in untreated arthritics. Lupus Erythematosus cell prevalence was found to be higher in untreated arthritics having a percentage Lupus Erythematosus test positivity of 6.8% compared to the 2.1% seen in treated arthritics. Conclusion: It was found that Autoimmunity in arthritics can be significantly lowered through treatment with Arthritic drugs, diets, life style modifications over a period of time. The study suggests that Antinuclear antibody and Lupus Erythematosus estimations could be adopted as markers of diagnosis, prognosis and monitoring of arthritis.
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Samycia, Michael, Collette McCourt, Kam Shojania, and Sheila Au. "Experiences From a Combined Dermatology and Rheumatology Clinic." Journal of Cutaneous Medicine and Surgery 20, no. 5 (July 8, 2016): 486–89. http://dx.doi.org/10.1177/1203475416649138.

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Background: The Dermatology and Rheumatology Treatment Clinic is a novel multidisciplinary clinic where patients are concomitantly assessed by a rheumatologist and dermatologist. Objectives: To determine the number of patients seen in clinic, patient demographics, and most common diagnoses. Method: A retrospective review was performed over a 2-year period. Data collected included patient age, sex, dermatologic diagnosis, rheumatologic diagnosis, biopsies performed, and number of follow-up visits. Results: A total of 320 patients were seen (78% female, 22% male). The most common rheumatologic diagnoses were systemic lupus erythematosus (18%), rheumatoid arthritis (15%), psoriatic arthritis (13%), and undifferentiated connective tissue disease (8%). The most common dermatologic diagnoses were dermatitis (17%), psoriasis (11%), cutaneous lupus (7%), various types of alopecia (6%), and infections (5%). Conclusions: Skin diagnoses were often unrelated to the underlying rheumatologic diagnosis. Rheumatologists and dermatologists can both benefit from being aware of the dermatologic conditions that rheumatologic patients are experiencing.
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Snaith, M. "Clinical Rheumatology: Established Rheumatoid Arthritis." Foot 10, no. 2 (June 2000): 113–14. http://dx.doi.org/10.1054/foot.2000.0598.

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Iyer, Deepa, and Ernest Wong. "Images in rheumatology: “Accelerator” arthritis." Indian Journal of Rheumatology 6, no. 3 (September 2011): 148. http://dx.doi.org/10.1016/s0973-3698(11)60079-4.

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Kiely, Patrick D. W., and Mark E. Lloyd. "Ankle arthritis – an important signpost in rheumatologic practice." Rheumatology 60, no. 1 (October 24, 2020): 23–33. http://dx.doi.org/10.1093/rheumatology/keaa531.

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Abstract Ankle arthritis is a useful clinical signpost to differential diagnosis in rheumatic disease. Biomechanical features and differences in cartilage physiology compared with the knee may confer protection of the ankle joint from factors predisposing to certain arthritides. The prevalence of ankle OA is low, and usually secondary to trauma. Primary OA of the ankle should be investigated for underlying causes, especially haemochromatosis. New presentations of inflammatory mono/oligo arthritis involving the ankle are more likely due to undifferentiated arthritis or spondyloarthritis than RA, and gout over CPPD. The ankle is often involved in bacterial and viral causes of septic arthritis, especially bacterial, chikungunya and HIV infection, but rarely tuberculosis. Periarticular hind foot swelling can be confused with ankle arthritis, exemplified by Lofgren’s syndrome and hypertrophic osteoarthropathy where swelling is due to subcutaneous oedema and osteitis respectively, and the ankle joint is rarely involved.
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Schwarting, Andreas. "Von ADAPTHERA zu Rheuma-VOR: Konzept der koordinierten Kooperation zur Verbesserung der rheumatologischen Versorgungsqualität." Aktuelle Rheumatologie 43, no. 05 (October 2018): 406–9. http://dx.doi.org/10.1055/a-0658-1031.

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ZusammenfassungRheumatologische Erkrankungsbilder nehmen in Ihrer Relevanz immer weiter zu. Die Kombination aus einem optimalen Behandlungsbeginn innerhalb von 12 Wochen nach Beschwerdebeginn und dem Mangel an Rheumatologen stellt eine große Herausforderung für alle Beteiligten dar. Ein möglicher Ansatzpunkt ist die koordinierte Kooperation von Patienten, Primärversorgern (Internisten, Orthopäden, Dermatologen) und den niedergelassenen Rheumatologen mithilfe einer zentralen Koordinationsstelle. Das erfolgreich etablierte rheinland-pfalzweite Netzwerk ADAPTHERA konnte zeigen, dass durch Risikostratifizierung eine zeitnahe Diagnose der Rheumatoiden Arthritis möglich ist und dabei die Ressource „Rheumatologe“ geschont wird. Die durch den Innovationsfonds des Gemeinsamen Bundesausschusses geförderte Proof-of-Concept Folgestudie Rheuma-VOR fußt auf dem gleichen Prinzip, jedoch stehen nun 3 entzündlich-rheumatische Erkrankungen (Rheumatoide Arthritis, Psoriasis Arthritis und Spondylarthritis) im Fokus. Zudem wurde das Projekt auf die Bundesländer Rheinland-Pfalz, Niedersachsen und dem Saarland ausgeweitet. Das Ziel ist die Steigerung der Versorgungsqualität in den 3 Bundesländern bei gleichzeitiger Reduktion der Wartezeiten.
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Dorst, Daphne N., Mark Rijpkema, Marti Boss, Birgitte Walgreen, Monique M. A. Helsen, Desirée L. Bos, Maarten Brom, et al. "Targeted photodynamic therapy selectively kills activated fibroblasts in experimental arthritis." Rheumatology 59, no. 12 (July 30, 2020): 3952–60. http://dx.doi.org/10.1093/rheumatology/keaa295.

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Abstract Objective In RA, synovial fibroblasts become activated. These cells express fibroblast activation protein (FAP) and contribute to the pathogenesis by producing cytokines, chemokines and proteases. Selective depletion in inflamed joints could therefore constitute a viable treatment option. To this end, we developed and tested a new therapeutic strategy based on the selective destruction of FAP-positive cells by targeted photodynamic therapy (tPDT) using the anti-FAP antibody 28H1 coupled to the photosensitizer IRDye700DX. Methods After conjugation of IRDye700DX to 28H1, the immunoreactive binding and specificity of the conjugate were determined. Subsequently, tPDT efficiency was established in vitro using a 3T3 cell line stably transfected with FAP. The biodistribution of [111In]In-DTPA-28H1 with and without IRDye700DX was assessed in healthy C57BL/6N mice and in C57BL/6N mice with antigen-induced arthritis. The potential of FAP-tPDT to induce targeted damage was determined ex vivo by treating knee joints from C57BL/6N mice with antigen-induced arthritis 24 h after injection of the conjugate. Finally, the effect of FAP-tPDT on arthritis development was determined in mice with collagen-induced arthritis. Results 28H1-700DX was able to efficiently induce FAP-specific cell death in vitro. Accumulation of the anti-FAP antibody in arthritic knee joints was not affected by conjugation with the photosensitizer. Arthritis development was moderately delayed in mice with collagen-induced arthritis after FAP-tPDT. Conclusion Here we demonstrate the feasibility of tPDT to selectively target and kill FAP-positive fibroblasts in vitro and modulate arthritis in vivo using a mouse model of RA. This approach may have therapeutic potential in (refractory) arthritis.
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Yehudina, Ye D., and S. А. Trypilka. "Paraneoplastic arthritis — at the crossroads of rheumatology and oncology." PAIN, JOINTS, SPINE 12, no. 1 (October 23, 2022): 23–29. http://dx.doi.org/10.22141/pjs.12.1.2022.325.

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Paraneoplastic arthritides (PA) are a group of inflammatory arthropathies associated with latent or manifest malignancy, localized in a distant site in relation to the primary focus and caused by immune-mediated mechanisms. Although the pathogenesis of PA is unknown, immune-mediated mechanisms can cause paraneoplastic syndrome with a dominant feature of polyarthritis. Arthritis can be both the initial manifestation of the disease, and it can manifest itself some time before the oncological process. Common forms of PA include paraneoplastic oligo/polyarthritis; hypertrophic osteoarthropathy; remitting seronegative symmetric synovitis with pitting edema; palmar fasciitis and pancreatic panniculitis associated with pancreatic carcinoma. The purpose of this review article was to describe the clinical characteristics, diagnostic assessment and treatment of paraneoplastic arthritis, and highlight the challenges that healthcare professionals may face in order to distinguish these conditions from other autoimmune rheumatic diseases. Further research is needed to understand the mechanisms associated with PA and to develop new diagnostic biomarkers.
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Solomon, Daniel H., Richard J. Bucala, Mariana J. Kaplan, and Peter A. Nigrovic. "Arthritis & Rheumatology : Evolving to Meet the Challenges of Rheumatology." Arthritis & Rheumatology 72, no. 8 (June 8, 2020): 1254–55. http://dx.doi.org/10.1002/art.41303.

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Dissertations / Theses on the topic "Rheumatology and arthritis"

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Newbold, David Anthony. "An evaluation of the rheumatology nurse practitioner." Thesis, King's College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263598.

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Hewlett, Sarah. "Values, disability and personal impact in rheumatoid arthritis." Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310640.

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Wang, Hui. "Modulation by transforming growth factor-#beta#1 and insulin-like growth factor-1 of cartilage collagen breakdown induced by pro-inflammatory cytokines." Thesis, University of Newcastle Upon Tyne, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327213.

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Arican, Mustafa. "Bone and cartilage metabolism in canine arthropathies." Thesis, University of Liverpool, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283505.

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Cresswell, Lynne. "Statistical modelling in rheumatology : applications to Psoriatic Arthritis and Systemic Lupus Erythematosus." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608755.

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Steel, Kathryn Jean Audrey. "Characterisation of a susceptibility locus for inflammatory arthritis." Thesis, University of Manchester, 2014. https://www.research.manchester.ac.uk/portal/en/theses/characterisation-of-a-susceptibility-locus-for-inflammatory-arthritis(0265f2ef-14ef-4d2a-979d-69a06b860324).html.

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Inflammatory arthritis (IA) types such as rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA) and psoriatic arthritis (PsA) have been shown to exhibit common clinical features. As complex diseases they have a known genetic component, some of which is known to be shared. The aim of this study was to assess the genetic overlap between 3 types of IA (RA, JIA and PsA) using genotype data generated on the Immunochip array and to select a biologically promising overlapping region for further genetic and functional investigation. Overlap analysis was performed using association data generated for a large cohort of inflammatory arthritis cases and shared controls (11,475 RA; 2816 JIA; 929 PsA respectively). 50 genetic regions were identified as being associated with more than 1 type of IA (p < 1x10-3), with several interesting similarities and differences observed between the diseases. As several of the overlapping regions detected represented novel disease associations, they required replication in an independent sample cohort. 12 variants were selected for replication in an independent RA cohort of 3879 cases and 2561 controls. Of these, 2 variants in the CTLA4 and MTMR3 regions were successfully replicated in RA at p<0.05. Bioinformatics analysis was performed for the 50 overlapping regions, with one particularly promising region, RUNX1, selected for further investigation. In this region, the same variant (rs9979383) is associated across the 3 diseases, with similar odds ratios (OR 0.8-0.9) observed in each disease. As this region represented both a novel IA association and had not been densely genotyped on the Immunochip array, fine mapping was performed by genotyping 51 SNPS in 3491 cases and 2359 controls. This resulted in replication of the association at rs9979383 (p=0.02) with no additional significant genetic effects detected, therefore this variant was selected for further functional analysis. As rs9979383 lies ~280kb upstream of the RUNX1 gene, a cis-eQTL analysis was performed to identify if the variant acts by regulation of RUNX1 gene expression. This was performed in whole blood, CD4+ and CD8+ lymphocytes from 75 (and a subset of 23) healthy volunteers respectively. No significant eQTLs were detected between rs9979383 and RUNX1 in whole blood (p =0.9) or RUNX1/LOC100506403 CD4+ and CD8+ lymphocytes (p=0.1). This study has provided insight into the genetic similarities and differences between different types of inflammatory arthritis, which can be applied to further investigations into disease susceptibility. Although no significant cis-eQTL was detected in any of these tissues with either RUNX1 or the nearby lnc-RNA LOC100506403, in cells from healthy volunteers under unstimulated conditions, these findings will direct future functional investigations into the role of this overlapping region in the susceptibility of IA.
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Ångström, Lars. "Aerobic capacity in rheumatoid arthritis : aspects of associations with cardiovascular risk factors and disease activity." Licentiate thesis, Umeå universitet, Reumatologi, 2018. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-164592.

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Rheumatoid arthritis (RA) is a systemic and inflammatory disease that has been associated with an increased morbidity and mortality in cardiovascular disease (CVD). Low aerobic capacity is one of the strongest independent risk factors for CVD and all-cause mortality in the general population. In patients with longstanding RA, low aerobic capacity has been related with a worse cardiovascular profile and an increased risk of CVD mortality. As a consequence of this, low aerobic capacity might provide an additional risk factor for CVD in patients with RA. The aim of this thesis was to describe the associations between aerobic capacity and risk factors for CVD as well as disease activity in patients with early RA, and also the effects of intensive exercise therapy on traditional risk factors for CVD and disease activity in patients with longstanding RA. Paper I, a cross-sectional study including 67 patients with early RA, mean (SD) age 53.1 (14.4), assessments of aerobic capacity, CVD risk factors, disease activity and functional ability were taken. Data were analysed for the associations between aerobic capacity and CVD risk factors and disease activity. In paper II, an intervention study, including 13 patients with RA, median age (Q1-Q3) 57 (44-64) years, aerobic capacity, pulse wave analysis (PWA), CVD risk factors, and disease activity were analysed for changes after 10 weeks of intensive exercise therapy. Additional follow-up was made after 25 weeks. In paper I, the mean (SD) aerobic capacity was 31.6 (8.7) ml O2/kg/min. CVD risk factors and disease activity were all in favour of patients with higher aerobic capacity. In a multiple regression model, adjusted for age and sex, aerobic capacity was significantly associated with percent body fat (β=-0.502, 95%CI=-0.671;-0.333) and triglycerides (β=-2.365, 95%CI=-4.252;-0.479). In paper II, intensive exercise over ten weeks was shown to be a feasible method to significantly improve aerobic capacity (p=≤0.05), systolic blood pressure (p=≤0.01) and the number of tender joints (p=≤0.05). No detrimental effect on disease activity was recorded. This thesis adds further knowledge of aerobic capacity and its associations with CVD risk factors and disease activity in patients with RA. Also, intensive exercise therapy was a feasible intervention to improve CVD risk factors. To include assessment of aerobic capacity in regular clinical practice may improve patient management as well as patient outcome in patients with RA.
Bakgrund: Reumatoid artrit (RA, ledgångsreumatism) är en kronisk inflammatorisk sjukdom som i första hand angriper leder, men kan även påverka inre organ. Typiska symptom är ledsvullnad, smärta, morgonstelhet och nedsatt funktion i lederna. Patienter med RA har visat sig ha en ökad risk att insjukna i och avlida i hjärt- och kärlsjukdom. I den allmänna befolkningen har låg syreupptagningsförmåga (kondition) visat sig vara en av de starkaste riskfaktorerna för att insjukna i eller att avlida i hjärt- och kärlsjukdom. Tidigare studier har visat att patienter med RA kan ha låg kondition vilket kan utgöra en riskfaktor för hjärt- och kärlsjukdom även vid RA. Syfte: Syftet med denna avhandling var att beskriva sambanden mellan kondition och riskfaktorer för hjärt- och kärlsjukdom och sjukdomsaktivitet. Ett annat syfte var att studera hur intensiv cykelträning påverkar kondition, traditionella riskfaktorer och sjukdomsaktivitet hos patienter med RA. Metod: Studie I är en tvärsnittsstudie, bestånde av 67 patienter med tidig RA, som hade en medelålder på 53 år. De undersöktes avseende; kondition, riskfaktorer för hjärt- och kärlsjukdom och sjukdomsaktivitet för att analysera samband mellan dessa. Studie II är en träningsstudie, bestående av 13 patienter med RA, med en medianålder på 57 år. Kondition, riskfaktorer för hjärt- och kärlsjukdom och sjukdomsaktivitet analyserades för att se förändringar efter tio veckors intensiv cykelträning samt vid en uppföljning efter 25 veckor. Resultat: I studie I visade den studerade gruppen ett konditionsmedelvärde på 31.6 mL. Sambandsanalyser visade att högre kondition var relaterad till lägre grad av riskfaktorer för hjärt- och kärlsjukdom, samt lägre 10 års risk för hjärt- och kärlsjukdom och sjukdomsaktivitet. I studie II fann vi att tio veckors intensiv cykelträning kan vara en användbar metod för att förbättra kondition, blodtryck och antalet ömma leder. Ingen ökad sjukdomsaktivitet noterades. Slutsatser: Dessa studier bidrar med kunskap om samband mellan kondition och riskfaktorer för hjärt- och kärlsjukdom samt sjukdomsaktiviteten hos patienter med RA. De visar också att intensiv cykelträning kan vara en effektiv metod att förbättra kondition och blodtryck hos patienter med RA.
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Kelly, Stephen Gerard. "Ultrasound imaging of synovitis : relationship to pathobiology and response to therapy." Thesis, Queen Mary, University of London, 2014. http://qmro.qmul.ac.uk/xmlui/handle/123456789/9010.

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Ultrasound (US) imaging has made significant progress over the past 20 years in relation to its role in inflammatory arthritis, and in particular, Rheumatoid Arthritis. Modern US machines provide crisp, detailed images of superficial anatomical structures which has facilitated the uptake of US imaging as an important assessment tool within the Rheumatology department. Diagnostic and prognostic information can now assist clinicians decisions with the goal of improving patient treatment and subsequent outcome. In addition, 3D US imaging has recently been suggested as an additional imaging modality with potential benefits in the assessment of in?ammatory arthritis. Recent work has focused on providing a reliable, responsive US joint count which can be assimilated into routine care as well as providing a platform for clinical research. Thus, my first aim was to show that a defined limited US data set, including 2D and 3D imaging, shows acceptable reliability. I demonstrate that both imaging modalities are reliable in terms of reading and image acquisition when restricted to a limited US data set. My second aim, was to demonstrate that a limited US data set is responsive. Using both a physiological and pharmacological trigger, I demonstrate that both 2D and 3D imaging are responsive and that combining US endpoints with DAS28 (Disease Activity Score - 28) increased the effect size and identifies treatment effects early. Despite notable advances in musculoskeletal US research, there is still need for better understanding of the pathophysiological correlates of ultrasound imaging. Therefore my final aim was to examine the relationship of Power Doppler Signal (PDS) and gray-scale synovial thickening with histological features of synovitis at a single joint level and with an extended joint US data set. I Firstly show that the harvesting of synovial tissue, using a minimally invasive US-guided biopsy technique, is safe and well tolerated by patients and that the quality of tissue and RNA extracted is good. Using this tissue collection method, I demonstrate a good correlation of US and histological parameters of synovitis (specifically CD68+ sub-lining macrophages) at a single joint level, in both an early and established RA cohort. This relationship is maintained if the US assessment is extended to a discrete US joint data set. Furthermore, within the knee joint I demonstrated that PDS correlates well with synovial tissue expression of inflammatory mediators of neoangiogenesis and histological assessment of synovial vascular area.
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Rathbun, Alan M. "Depression in Rheumatoid Arthritis and an Estimation of the Bi-directional Association of Depression and Disease Burden: A Dissertation." eScholarship@UMMS, 2014. http://escholarship.umassmed.edu/gsbs_diss/699.

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Depression is a common comorbidity in rheumatoid arthritis (RA), yet it may not be adequately recognized during routine clinical care. RA symptoms may confer a risk for depression, and vice versa; depression may affect RA disease activity and response to treatment. The study aims were to compare patient- and physician-reported depression measures, evaluate the temporal bi-directional association between RA disease activity and depressive symptomology, and assess depression as a moderator of RA treatment. Patients were identified using a national RA registry sample (Consortium of Rheumatology Researchers of North America; CORRONA). Depression prevalence and incidence rates were estimated, and concordance and disagreement using measures reported separately by patients and physicians, as well as baseline cross-sectional associations between RA disease and a history of depression. A survival analysis was conducted to temporally predict the incident onset of self-reported depressive symptoms using the different metrics of RA disease activity. Also, mixed effects models were used to assess prospective changes in RA disease activity by prevalent and incident depressive symptom status. Lastly, logistic regression models compared the likelihood of clinical response to RA treatment during follow-up in those with and without depression when starting biologic disease modifying anti-rheumatic drug (DMARD) therapy. Patient-reported depression rates were much higher and significantly different from physician based comorbidity estimates. Patient and physician RA disease activity measures were associated with an increased risk for depression onset, but not laboratory-reported serum biomarkers. Similarly, depression was temporally associated with significantly slower rates of decline regarding every patient-reported disease activity measure, some physician-reported metrics, but not acute phase reactants. Moreover, there was a significantly lower probability of achieving clinical remission among those with depression on a biologic DMARD after 6 months and an analogous effect at 12-months that was slightly lower in magnitude, which did not reach statistical significance. Rheumatologists under-reported the occurrence of prevalent and incident depressive symptoms, and thus are likely unaware of its presence in their RA patients. Further, the results suggest the bi-directional effects between these conditions are related to the cognitive and behavioral aspects of depression and their interactions with disease activity, rather than shared immunological mechanisms in the context of cell-mediated immunity. When also considering the impact on clinical response to biologic DMARDS, the findings collectively imply that rheumatologists must address any challenges due to depression to provide the best care to their patients.
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Humphreys, Jennifer. "Validation of the 2010 American College of Rheumatology/European League Against Rheumatism classification criteria for rheumatoid arthritis with special emphasis on the role of autoantibodies." Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/validation-of-the-2010-american-college-of-rheumatology-european-league-against-rheumatism-classification-criteria-for-rheumatoid-arthritis-with-special-emphasis-on-the-role-of-autoantibodies(189200f1-4daa-4c99-8019-9b600c03ee0c).html.

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Aim: The aim of this thesis was to validate the 2010 American College of Rheumatology/European League Against Rheumatism classification criteria for rheumatoid arthritis (RA), in particular with respect to its construct validity and the role of autoantibodies within the criteria. Methods: This thesis used data from the Norfolk Arthritis Register, a longitudinal inception cohort of adults (16 years and over) with inflammatory polyarthritis (IP), defined as at least 2 swollen joint for at least 4 weeks. The 2010 criteria were used to define RA, firstly in a re-estimation of the incidence rates (IR) with comparisons made to incidence defined by the previous criteria set; and secondly in a study comparing mortality rates in patients with RA to those of the general population, and how these rates changed over time. Analyses were performed testing the ability of the 2010 criteria to identify those patients with IP at increased risk of mortality, disability, disease severity and radiographic damage. The levels and number of autoantibodies present were investigated as predictors of mortality in patients with IP. The association between anti-carbamylated protein (anti-CarP) antibodies and long term disease outcomes were investigated. Results: The incidence of RA was 40 per 100 000 population; baseline IRs were similar to the cumulative IRs using the previous criteria set over 5 years. Patients who were seronegative were less likely to be classified as RA by the 2010 criteria. Mortality rates in patients with RA were higher compared to the general population (standardised mortality ratio 1.16, 95 percent confidence interval (CI) 1.04-1.29) and declined over the study period at the same rate as the general population. Patients with IP who fulfilled the 2010 criteria had increased risk of early death (hazard ratio (HR) 1.35, 95 percent CI 1.13-1.64), as well as increased levels of disability (beta 0.38, 95 percent CI 0.33-0.43), disease severity (beta 1.63, 95 percent CI 1.54-1.73) and radiographic damage (beta 0.33, 95 percent CI 0.20-0.47) throughout follow up. Patients with two autoantibodies had an increased risk of early death (HR 1.35, 95 percent CI 1.09-1.68), but there was no association with early death and the levels of these antibodies. Anti-CarP antibody positivity was independently associated with worse disability (beta 0.12, 95 percent CI 0.02-0.21) and disease severity (beta 0.23, 95 percent CI 0.07-0.39) throughout follow up. Conclusions: The 2010 ACR/EULAR classification criteria for RA identify patients with IP early in their disease course and recognise those at increased risk of mortality and poor outcomes. The 2010 criteria may miss a subgroup of seronegative patients who nevertheless have a poor prognosis. Novel autoantibodies may be useful to identify this subgroup.
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Books on the topic "Rheumatology and arthritis"

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Clarke, Amy Key. Rheumatology. Tunbridge Wells: Castle House Publications, 1986.

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Clarke, A. K. Rheumatology. Tunbridge Wells: Castle House, 1986.

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Fauci, Anthony S. Harrison's rheumatology. Edited by Harrison Tinsley Randolph 1900-1978. 3rd ed. New York: McGraw-Hill Medical, 2013.

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Campion, G. V. Rheumatology. Oxford: Blackwell Scientific, 1989.

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J, Koopman William, ed. Clinical rheumatology. Philadelphia: Saunders, 1986.

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Campion, Giles. Rheumatology. 2nd ed. Oxford: Blackwell Scientific, 1996.

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Moll, J. M. H. Rheumatology. 2nd ed. Edinburgh: Churchill Livingstone, 1997.

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Rheumatology. Edinburgh: Churchill Livingstone, 1992.

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Dick, W. Carson. Introduction to clinical rheumatology. Edinburgh: Churchill Livingstone, 1985.

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1939-, Kelley William N., ed. Textbook of rheumatology. 3rd ed. Philadelphia: Saunders, 1989.

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Book chapters on the topic "Rheumatology and arthritis"

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Helliwell, Philip S., Howard A. Bird, and Verna Wright. "Rheumatoid Arthritis." In Rheumatology, 3–22. London: Springer London, 1989. http://dx.doi.org/10.1007/978-1-4471-1691-2_1.

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Helliwell, Philip S., Howard A. Bird, and Verna Wright. "Juvenile Arthritis." In Rheumatology, 56–62. London: Springer London, 1989. http://dx.doi.org/10.1007/978-1-4471-1691-2_4.

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Helliwell, Philip S., Howard A. Bird, and Verna Wright. "Seronegative Arthritis." In Rheumatology, 64–86. London: Springer London, 1989. http://dx.doi.org/10.1007/978-1-4471-1691-2_5.

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Handa, Rohini. "Psoriatic Arthritis." In Clinical Rheumatology, 81–86. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-33-4885-1_8.

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Handa, Rohini. "Rheumatoid Arthritis." In Clinical Rheumatology, 51–65. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-33-4885-1_6.

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Handa, Rohini. "Viral Arthritis." In Clinical Rheumatology, 215–19. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-33-4885-1_28.

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Handa, Rohini. "Reactive Arthritis." In Clinical Rheumatology, 87–89. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-33-4885-1_9.

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Handa, Rohini. "Seronegative Arthritis." In Clinical Rheumatology, 91–93. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-33-4885-1_10.

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van der Pouw Kraan, Tineke C. T. M., Lisa G. M. van Baarsen, François Rustenburg, Belinda Baltus, Mike Fero, and Cornelis L. Verweij. "Gene Expression Profiling in Rheumatology." In Arthritis Research, 305–27. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-402-5_22.

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Helliwell, Philip S., Howard A. Bird, and Verna Wright. "Immunology and Infectious Arthritis." In Rheumatology, 24–34. London: Springer London, 1989. http://dx.doi.org/10.1007/978-1-4471-1691-2_2.

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Conference papers on the topic "Rheumatology and arthritis"

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Reddy, Narender P., Ekta Shah Dharaiya, and Bruce M. Rothschild. "Noninvasive Acceleration Measurements of Physiological Vibrations: Assessment of Finger Arthritis." In ASME 2011 International Mechanical Engineering Congress and Exposition. ASMEDC, 2011. http://dx.doi.org/10.1115/imece2011-65067.

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Noninvasive measurements are fast gaining importance in every clinical discipline. Noninvasive acceleration measurements of physiological vibrations may aid in clinical diagnosis and quantitative assessment of various diseases. In the discipline of rehabilitation medicine, Reddy et al [1–4] have developed and clinically evaluated the techniques of non-invasive quantitative assessment of the swallowing mechanism in dysphagic patients, using noninvasive measurements of acceleration at the throat. In the discipline of rheumatology, Reddy et al.[5] have used acceleration signals to distinguish osteoarthritis, rheumatoid arthritis, and chondromalacia of the knee joint. Rangayyan et al [6] have used acceleration signals from the knee joint to classify articular cartilage pathology. Reddy et al [7] have reported measurement of acceleration for differential diagnosis of spondylo-arthropathy from rheumatoid arthritis of the knee joint.
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SILVA, ICARO CRUZ, MARILIA VIEIRA FEBRÔNIO, WILLIAN MORORO LIMA, LUANN SOARES NUNES, PAULO ANTONIO DAMIÃO SANTOS, CRISTIANO GEORGE CAMOS HEINZEL, MATHEUS ALMEIDA ARAUJO, ROMARIO LIMA DANTAS, ALEXANDRE TELES CORUMBA, and FERNANDO ANTONIO CHAGAS COELHO. "JUVENILE IDIOPATHIC ARTHRITIS IN A PEDIATRIC RHEUMATOLOGY SERVICE, ARACAJU, SERGIPE." In 36º Congresso Brasileiro de Reumatologia. São Paulo: Editora Blucher, 2019. http://dx.doi.org/10.5151/sbr2019-493.

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Maschio, M., S. Pieropan, F. Caldonazzi, G. Dallagiacoma, V. Ravagnani, D. Degani, G. Piacentini, D. Biasi, and M. Rossini. "AB0953 Arthritis following parasitic infection in the differential diagnosis of juvenile idiopathic arthritis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.4876.

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Storkanova, H., K. Bubova, S. Oreska, M. Spiritovic, B. Hermankova, M. Gregorova, K. Mintalova, et al. "P171 Hsp90 in axial spondyloarthritis, psoriatic arthritis and rheumatoid arthritis." In 39th European Workshop for Rheumatology Research, 28 February–2 March 2019, Lyon, France. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2019.153.

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Freeston, JE, KS Mankia, M.-A. D'Agostino, R. Hodgson, A. Grainger, I. Matsuura, N. Larkman, PG Conaghan, and P. Emery. "FRI0630 Can whole body mri at baseline identify definite inflammatory arthritis patterns in undifferentiated arthritis?" In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.5051.

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Miyachi, K., A. Ihara, and B. Sasse. "THU0695 Does hormone replacement therapy prevent undifferentiated arthritis progressing to rheumatoid arthritis." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.4077.

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Iwakura, Y. "SP0003 Novel animal model in arthritis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.7154.

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Jager, W. de. "SP0067 Cytokines in juvenile idiopathic arthritis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.7203.

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Hugues, B., S. Hilliquin, S. Mitrovic, L. Gossec, and B. Fautrel. "OP0011 Does a very early therapeutic intervention in very early arthritis / pre-rheumatoid arthritis patients prevent the onset of rheumatoid arthritis: a systematic review and metanalysis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.5323.

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Szentesi, Margit, Zoltán Nagy, Zsolt Karoly Mangel, and Pál Géher. "AB0447 BIOLOGICAL THERAPY AND RADIOSYNOVIORTHESIS IN PATIENTS WITH RHEUMATOID ARTHRITIS AND PSORIATIC ARTHRITIS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.3071.

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Reports on the topic "Rheumatology and arthritis"

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Russell, Mark, James Galloway, Sumera Qureshi, Joanna Ledingham, Arti Mahto, Andrew Rutherford, Maryam Adas, et al. Incidence and management of inflammatory arthritis in England before and during the COVID-19 pandemic. OpenSAFELY, January 2023. http://dx.doi.org/10.53764/rpt.ca5bce7991.

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The National Early Inflammatory Arthritis Audit (NEIAA) is the largest audit of its kind globally, reporting on care delivered across rheumatology services in the NHS in England. Clinical researchers from King’s College London are collaborating with OpenSAFELY to recreate key aspects of NEIAA, and benchmark the quality of care for people with inflammatory arthritis in England. This report will be updated on a regular basis.
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