一.背景 痛风性关节炎，属于中医“痹证”“白虎历节风”“痛风”范畴。是以高尿酸血症为生化基础，继发尿酸盐结晶沉积、关节损害、结石形成所致的急慢性关节炎，表现为关节红、肿，疼如刀绞，痛剧难忍，亦可自行缓解，常发作无常，来去如风，故名痛风，是痛风病的中、后期阶段。严重者可造成骨质破坏、关节畸形。 本病受遗传、环境和饮食习惯的影响，患病率逐年增加。现代医学治疗本病，急性期以控制症状，减轻痛苦；缓解期以降低高尿酸血症为目标，尚无根治方法；况且所用药物均有较大的毒副反应，使本病的治疗处于窘境。中医中“痛风”之名始於金元，由朱丹溪首先提出，并设专篇论述，其在〈格致余论－痛风〉中指出“痛风者，四肢百节走痛，书中谓之白虎历节风证是也”“大率因血受热，已自沸腾，其后或涉冷水，或立湿地，或扇风取凉，或卧地当风，寒凉外搏，热血得寒，污浊凝瑟所以作痛，夜则痛甚，行于阴也”。其发病以脾肾两虚为本，湿、 热、毒、为标，热毒重可生湿，湿邪盛能化热，内毒流窜经络，攻注骨节，着于经脉，终致湿热毒交互为患，证属正虚邪实。近年来中医药对痛风研究逐渐深入，主要为中药汤剂的研究较为广泛，关于针灸、推拿、拔罐等中医传统特色治疗研究逐步开展，并取得可喜成绩。 二．目的 本次研究拟通过对现有关于痛风性关节炎中医手段治疗的临床研究类文献和实、验研究类文献的搜集、整理、分析，从而对痛风性关节炎中医治疗手段的临床有效率进行统计，并对痛风性关节炎中医治疗手段的改进与发展进行探讨。 三．万法 本論文文献资料来源：中国期刊全文数据库（CNKI）。通过对中国期刊全文数据庫库（CNKI）进行标准检索，方法为：计算机检索2005年－2015年国内外关于痛风性关节炎的中医治疗文献，搜素关键宇：痛风性关节，并包含中医、中药、针刺 、针灸， gout 、gouty arthritis。 经过文章检索方法的纳入与排除，得到所研究的文献。 四,結果 搜索中医治疗痛风性关节炎综遮类文献356篇；中药类治疗文献493篇，其中中药内用临床研究类文献317篇、中药内用实验研究类文献176 篇、中药外敷类研究文献79篇；针刺、针灸类治疗研究文献183篇，排除重复19篇，剩余共计164篇。经纳入和排除后，共得可用文献145篇，其中痛风性关节炎证候分型、辩证论治类21篇，中药、针刺等各法临床类研究文献83篇，实验类研究文献4l篇。 在文献分析过程中得出结果：1.痛风性关节炎的证型为：湿热蕴结型、淤热阻滞型、痰浊阻滞型、肺气虚弱型、肝肾阴虚型等。2. 病情分期为：急性期、静止期、慢性期。3.（统计排位前三）中药内用常用方剂为：四妙九、上中下痛风汤、二陈汤；常用中药为：薏苡仁、黄柏、牛膝；常用药物类为：通络止痛类、清热燥湿解毒类、利湿化浊类；常用药对为：茯苓与薏苡仁、苍术与黄柏、山栀与黄柏；常用针刺术穴位：曲池、血海、三阴交。 研究文献中所有中医临床治疗方法均对痛风性失节炎有效，作用率100% 。并无毒、副作用。 五, 结论 中医治疗对于痛风性关节炎有良好的综合性治疗效果，强于口服西药。

Thesis (Masters Degree( Medical Technology) --Cape Technikon, Cape Town,1996 / Intensive investigations in many different populations over the last decade, have indicated a failure to understand the inheritance of rheumatoid arthritis (RA). It was hoped that genes within the class IT region of the major histocompatibility complex (MHq could shed some light on the inheritance of this autoimmune disease and which are now known without doubt, to confer susceptibility to the disease. Genetic studies of RA have concentrated primarily on its autoimmune nature and several investigations of MHC class IT molecules, have demonstrated an association between specific HIA alleles and susceptibility to RA, in particular the DRBI*04 and DRBI*01 alleles. - The HIA system is known to be associated with many diseases involving an immune aetiology. The structural features of specific DR and DQ genes give clues to the molecular mechanisms by which these alleles are associated with RA It has been found by many investigators that there is more than one susceptibility allele for RA at the DRBI locus. Questions arise whether the DRBI molecule itself directly contributes to the pathogenesis ofRA and why some DRBI genes carrying DRBI*04 alleles, are not associated withRA Animal studies have emphasised the critical importance of T-cells in the pathogenesis of RA Immune responsiveness is thought to be controlled by specific allelic variation by determining the ability of specific T-cell receptors (fCRs) to be triggered by recognition of class IT molecules during the induction of the immune response. In a disease such as RA, however, where multiple alleles are thought to confer risk, it is not yet known whether each of these alleles shares some common structural feature triggering a single T-cell pathway or whether each allele represents an alternative recognition site which triggers different T-cell clones, all of which lead to a similar clinical syndrome.

CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superior / Artrite à uma doenÃa inflamatÃria que afeta as articulaÃÃes sinoviais. Os sintomas mais comuns sÃo o aumento da sensibilidade à dor nas articulaÃÃes (hiperalgesia ou hipernocicepÃÃo) e edema. Uma alternativa para o tratamento da doenÃa à a inclusÃo de plantas medicinais. O Ãleo extraÃdo dos frutos do pequi (Caryocar coriaceum Wittm), tem ampla aplicabilidade na medicina popular. Ensaios prÃ-clÃnicos demonstraram propriedades terapÃuticas do Ãleo, tais como anti-inflamatÃria, gastroprotetora e cicatrizante. Com base neste contexto, o objetivo do presente estudo foi investigar a atividade antinociceptiva e anti-inflamatÃria do Ãleo de pequi (OPCC) na artrite induzida por zymosan em ratos. O estudo foi aprovado pela ComissÃo de Ãtica em Pesquisa Animal da Universidade Federal do Cearà (n 83/11). A artrite foi induzida por uma injeÃÃo intrarticular, no joelho direito, de zymosan (1mg/50ÂL) e foram avaliados a incapacitaÃÃo articular (hipernocicepÃÃo), edema articular, migraÃÃo de leucÃcitos, liberaÃÃo de citocinas e expressÃo de mediadores inflamatÃrios. Os animais foram prÃ-tratados, por via oral, com OPCC (100, 200 e 400mg/kg) ou veÃculo durante 7 dias consecutivos ou em dose Ãnica, 45 minutos, antes da induÃÃo de artrite. Dexametasona, indometacina ou dipirona foram utilizadas como controles positivos. A incapacitaÃÃo articular foi avaliada durante 4 horas apÃs a injeÃÃo de zymosan. Em seguida os animais foram eutanasiados, procedendo-se a lavagem da cavidade articular com EDTA em PBS para avaliaÃÃo de infiltraÃÃo de leucÃcitos, atividade de mieloperoxidase e dosagem de citocinas. O tecido sinovial foi colhido para anÃlise imunohistoquimica de TNF-&#945; e COX-2. TambÃm foram avaliados o edema (diÃmetro transversal da articulaÃÃo) e o aumento da permeabilidade vascular pelo mÃtodo de extravasamento do Azul de Evans. O efeito antinociceptivo foi avaliado ainda atravÃs do teste de hiperalgesia mecÃnica plantar (Von Frey eletrÃnico) utilizando carraginia e PGE2. Os resultados demonstraram uma diminuiÃÃo significativa (p<0,05) da incapacitaÃÃo articular de todos os grupos tratados com OPCC durante 7 dias, no entanto com a dose Ãnica apenas as doses maiores foram eficazes. Em relaÃÃo à migraÃÃo de leucÃcitos para o lÃquido sinovial todos os grupos tratados com o OPCC (dose Ãnica e doses diÃrias) apresentaram significativa reduÃÃo (p<0,05) do nÃmero de leucÃcitos no lavado articular, acompanhada de uma diminuiÃÃo (p<0,05) na atividade da mieloperoxidase. Observou-se uma diminuiÃÃo (p<0,05) da liberaÃÃo de citocinas (TNF-&#945; e IL-1&#946;) no lÃquido sinovial, assim como expressÃo de TNF&#945; e COX-2 no tecido sinovial. O edema foi inibido (p<0,05) com o tratamento com OPCC em todas as doses administradas diariamente. AlÃm disso, os grupos tratados com 100 e 400mg/kg de OPCC apresentaram uma reduÃÃo significativa (p<0,05) da permeabilidade vascular. Os resultados mostraram ainda que a OPCC reduziu significativamente (p < 0,05) a hipernocicepÃÃo induzida pela carragenina e PGE2. Os dados sugerem que o OPCC exibe efeito anti-inflamatÃrio evidenciado pelo modelo de artrite induzida por zymosan em ratos, que pode ser associada com a inibiÃÃo da produÃÃo de citocinas prÃ-inflamatÃrias (TNF-&#945; e IL-1&#946;). Aparentemente essa aÃÃo pode estar envolvida com a inibiÃÃo da migraÃÃo de neutrÃfilos. Sugerimos ainda que o OPCC previne o desenvolvimento da hipernocicepÃÃo inflamatÃria mecÃnica evocada por carragenina e PGE2 (bloqueio direto da hipernocicepÃÃo) em ratos. / Arthritis is an inflammatory disease that affects synovial joints. The most common symptoms are increased sensitivity to joint pain (hyperalgesia or hypernociception) and edema. An alternative to treating the disease is the inclusion of medicinal plants. The oil extracted from the fruits of Pequi (Caryocar coriaceum Wittm) has wide applicability in popular medicine. Pre-clinical tests have demonstrated the therapeutic properties of the oil, such as anti-inflammatory, gastroprotective and healing. Based on this background, the objective of this study was to investigate the antinociceptive and anti-inflammatory oil Pequi (OPCC) in zymosan-induced arthritis in rats. The study was approved by the Ethics Committee on Animal Research of the Federal University of Cearà (n 83/11). Arthritis was induced by intraarticular injection in right knee of zymosan (1mg/50ÂL) and evaluated the articular incapacitation (hypernociception), joint swelling, leukocyte migration, cytokine release and expression of inflammatory mediators. The animals were pretreated orally with OPCC (100, 200 e 400mg/kg) or carrier for 7 consecutive days either as a single dose 45 minutes before the induction of arthritis. Dexamethasone, indomethacin or dipyrone were used as positive controls. The articular incapacitation was assessed 4 hours after injection of zymosan. Then the animals were euthanized, proceeding to wash the joint cavity EDTA in PBS for evaluation of leukocyte infiltration, myeloperoxidase activity and cytokine. The tissue synovial fluid was harvested for immunohistochemical analysis of TNF-&#945; and COX-2. We also evaluated edema (transverse diameter of the joint) and increased vascular permeability by the method of Evans blue extravasation. The antinociceptive effect was evaluated further by testing plant mechanical hyperalgesia (von Frey electronic). The results showed a significant decrease (p <0.05) joint of disability in all groups treated with OPCC for 7 days, but with only a single dose, higher doses were effective. Compared to the migration of leukocytes into the synovial fluid all groups treated with the OPCC (single dose and daily doses) showed a significant reduction p <0.05) in the number of leukocytes in the BAL joints, accompanied by a decrease (p <0.05) in myeloperoxidase activity. There was a decrease (p <0.05) cytokine release (TNF-&#945; and IL-1&#946;) in the synovial fluid as well as expression of TNF and COX-2 in synovial tissue. The edema was inhibited (p <0.05) treatment with all doses in OPCC. Moreover, the groups treated with 100 and 400mg/kg of OPCC showed a significant reduction (p <0.05) in vascular permeability. The results also showed that the OPCC significantly reduced (p <0.05) hypernociception and PGE2 induced by carrageenan. The data suggest that the OPCC exhibits anti-inflammatory effect evidenced by arthritis model in rats induced by zymosan, which can be associated with the inhibition of the production of proinflammatory cytokines (TNF-&#945; and IL-1&#946;). Apparently this action may be involved in the inhibition of neutrophil migration. We also suggest that the OPCC hypernociception prevents the development of carragenan-evoked inflammatory mechanical and PGE2 (direct blockade of hypernociception) in rats.

Rheumatoid arthritis (RA) is a systemic, inflammatory disease, which predominantly affects multiple joints. RA is characterized by swollen joints and peri-articular bone erosion. Conventional RA treatments have shown to reduce inflammation and slow down bone erosion, but repair of bone erosion is limited. Additionally, failure to repair for bone erosion in rheumatoid arthritis (RA) is caused by inadequate osteoblast-mediated bone formation resulting from focal inflammatory environment. Hence, there is immediate need to facilitate greater insight and develop a new therapeutic strategy to aid osteoblast -mediated repair of bone loss in RA. CKIP-1 is an intracellular inhibitor, that can negatively regulate osteoblast lineage cells differentiation and activity. CKIP-1 levels were found to be aberrantly over expressed in bone specimens from RA patients and arthritis mice, which was associated with reduced bone formation and increased disease severity. By genetic approach, overexpressed CKIP-1 in osteoblast exacerbated bone erosion and articular inflammation in CIA mice, whereas deficiency of CKIP-1 in osteoblast alleviates bone erosion in CIA mice. By pharmacological approach, RNA interference-based silencing of osteoblastic CKIP-1 led to bone formation-mediated reparative process at erosive site and reduced articular inflammation in arthritis induced mice. To extend above findings to a more relevant species that more closely resemble humans, we aimed to investigate the role of osteoblastic Casein kinase-2 interacting protein-1 (CKIP-1) in failure to repair bone erosion in non-human primate (NHP) arthritis model in this study. We found that CKIP-1 mRNA expression in osteoblasts of arthritic NHP was significantly suppressed by CKIP-1 siRNA treatment. Moreover, silencing of CKIP-1 in osteoblast of arthritis monkey improved clinical signs such as reduction in arthritis score, joint swelling and increase in body weight. Similarly, suppression of osteoblastic CKIP-1 resulted in better organized bony and articular structure with, fewer bone erosion sites as observed in x ray and micro CT images. Moreover, we found increase in bone mass, bone formation parameters such as BFR/BS and MAR and histological examination revealed attenuation of peri articular bone erosion and intraarticular inflammation in CKIP-1 siRNA treated arthritis monkeys. Taken together, these data strongly suggest that highly expressed osteoblastic CKIP-1 plays an important role in failure to repair articular bone erosion by inhibiting bone formation in RA. Targeting osteoblastic CKIP-1 could serve as a new therapeutic strategy by bone repair augmentation in RA.

Class of 2005 Abstract / Objectives: To evaluate potential productivity differences among working-age individuals with arthritis in the United States, and to determine the costs associated with these differences. Methods: Health risk assessment survey data was obtained through the You First internet survey group. Five hundred seventy-nine individuals with and 579 without arthritis, matched for age, were evaluated for differences in survey responses. The arthritis group was also evaluated to determine the association of pain severity level and activity limitations with work days missed. Results: Arthritis respondents were found to have significantly more work days missed, emergency room visits, hospital visits, and physician visits than respondents without arthritis. Arthritis respondents missed 6.14 more work days in the 12 months before taking the survey than non-arthritis respondents, costing US $12.9 billion in the United States each year. Arthritis respondents were significantly more limited in their activities than non-arthritis respondents. Arthritis pain and activity limitation were found to be positively correlated with work days missed. Implications: The data from this study demonstrate that work productivity is impaired in individuals with arthritis, pain and physical activity limitations are positively correlated with missed work days, and missed work days constitute a substantial annual cost to employers. Given the evidence of costly productivity impairment in arthritis patients vs. a general population, lost productivity should be included with direct medical costs in studies determining the burden of arthritis in the United States, especially from the employer’s perspective.

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.

Motherhood has been described as an identity, a role, and a way of participating in life (Arendell, 2000; Farber, 2004). Motherhood has also been described as 'work', the care taking, nurturing and teaching of children (Francis-Connolly, 2000). Mothers with arthritis have reported difficulty in the tasks of parenting and household work (Allaire et al., 1991; Backman, Kennedy, Chalmers & Singer, 2004; Barlow, Cullen, Foster, Harrison & Wade, 1999; Grant, Cullen & Barlow, 2000; Reisine, Grady, Goodenow & Fifield, 1998), however, we know little about how a mother experiences these challenges. While the subjective experience of being a mother and having a disability is intrinsically linked to participation, health and social interaction (Farber, 2004), research has not been conducted on how mothers with arthritis experience mothering in the presence of arthritis, and how this experience affects their participation, identity and social interaction. This narrative research study asks "How is being a mother and doing motherhood activities affected by your arthritis?" Study objectives include: 1) Describe mothers' experiences of nurturing, teaching and caring for their children. 2) Describe how mothers understand and explain the effect of arthritis on their role of mother. 3) Describe whether or not this understanding changes how mothers participate and interact in their community. Narrative inquiry was used to explore the experiences of eight married mothers with inflammatory arthritis who have at least one child (aged 0-18) living at home. Purposive sampling allowed representation of families from different communities, with children of different ages. Data collection included two in-depth interviews, participant observation, document review, and fine art painting. Data was coded and analyzed using narrative inquiry techniques (Coffey & Atkinson, 1996; Riessman, 1993; Sandelowski, 1991). Overarching storylines are presented as narratives that describe the mother's experiences of identifying with the role of mother, participation, fatigue and the social context in which mothering occurs. This study contributes to the sparse body of literature on the impact of arthritis on participation in maternal practices and social interaction, informing health professionals about the experience of mothering with arthritis. / Medicine, Faculty of / Graduate

In order to provide adequate treatment facilities, the B.C. Division of the Canadian Arhtritis and Rheumatism Society made arrangements with the Western Society for Rehabilitation whereby twelve beds were reserved for the non-pay patients of the C.A.R.S. During the period of two years fifty-eight in-patients received treatment there. The relevance of casework for these patients is studied in the present thesis. The in-patients came from all parts of British Columbia and were selected on the basis of low income, favourable prognosis and certain requirements set by the policy of W.S.R. Because of these factors, this study is limited to a carefully selected group, and does not include patients whose illness was far advanced. Case illustrations are used to evaluate the effectiveness of services given. These also point up some of the special problems which this group has encountered. The nature of the illness and the need for a total approach in the rehabilitation process make it clear that the social worker is an indispensable member of the treatment team. This study shows also some of the factors which can hinder or prevent successful rehabilitation. Limitation in the physical setting, lack of funds, and lack of co-ordination of basic resources for treatment, re-education and follow-up, all detract from the potential effectiveness of the services so far available. Certain tentative recommendations are made on these points. Since arthritis is a condition about which medical science has not yet acquired a workable body of knowledge, this project must necessarily be somewhat exploratory. But the study leaves no doubt that the project undertaken by C.A.R.S. has made a significant contribution to the physical and mental well-being of the patients under treatment. / Arts, Faculty of / Social Work, School of / Graduate

Introduction: Rheumatoid arthritis (RA) is known to be associated with an increased risk of cardiovascular disease (CVD), resulting in excess mortality. Dyslipidaemia has been identified as a major CVD risk factor in the general population. Current evidence would suggest that lipid metabolism is altered in RA due to inflammation, and that use of anti-inflammatory therapy may reverse some of these changes. However, the impact of such lipid changes on CVD in RA remains unknown. Data regarding the effects of RA/drug therapy on lipid structure and function are sparse. Genetic factors are important in the pathogenesis of RA and play a central role in the regulation of lipid metabolism. To date, no studies have assessed the impact of genetic polymorphisms on lipids in RA.The aim of this thesis is to: 1) assess the prevalence of dyslipidaemia in RA and the CVD risk this confers 2) establish the effects of inflammation on lipid levels and lipid ratios 3) assess the impact of anti-inflammatory drug therapy (anti-TNF, rituximab and intravenous glucocorticoids) on lipid levels, structure and function 4) assess the prevalence and associations of particular genetic polymorphisms (RA susceptibility and lipid metabolism regulating genes) with lipids in RA.Methods: Data from 400 RA patients were used to address aims 1, 2 and 4 in cross-sectional studies. All patients had a clinical assessment and fasting blood taken. Blood was processed to provide data on the lipid profile, ESR, CRP and DNA was extracted for genotyping. Aim 2 and 4 also utilised a retrospective longitudinal cohort of 550 RA patients and the DNA from 400 healthy controls, respectively. Aim 3 was addressed using a longitudinal cohort including: patients due to commence anti-TNF (n=35), rituximab (n=10), intravenous glucocorticoids (n=12); 15 RA controls on stable therapy; and 40 healthy controls. Assessments and blood samples were taken at baseline, 2 weeks and 3 months. Results: Dyslipidaemia was highly prevalent (56.8%), but undertreated in many RA patients at risk of developing CVD. Systemic inflammation associated with many of the changes in lipid levels and structure. Lipid ratios were found to be less susceptible to fluctuations due to inflammation. The use of anti-inflammatory drug therapy produced changes in lipid structure and function through both generic suppression of inflammation and drug specific mechanisms (particularly in the case of glucocorticoids). The prevalence of cholesterol ester transfer protein (CETP) and Apolipoprotein C3 genetic polymorphisms differed between RA patients and local population controls. RA susceptibility genes (HLA-DRB1-SE and TRAF1C5) and several ’lipid metabolism genes’ (Apolipoprotein E, ATP-binding cassette transporter 1 (ABCA1) and CETP) were found to associate with lipid levels within the RA population. Conclusion: Dyslipidaemia is highly prevalent in RA and currently undertreated. Dyslipidaemia in RA is regulated by numerous factors including inflammation, drug therapy and genetic factors. Further longitudinal studies are required to assess whether these findings have an impact on hard CVD endpoints.

Introduction: Rheumatoid arthritis (RA) is a systemic autoimmune condition, characterised by an inflammatory arthritis. It is associated with a 50% increased risk of cardiovascular (CV) mortality. Chronic inflammation is thought to lead to accelerated atherosclerosis in RA. There is some evidence to suggest that patients have a more inflammatory, unstable atherosclerotic plaque phenotype. The impact of advances in RA treatment, on cardiovascular co-morbidity remains unclear. The aims of the current study were to employ non-invasive imaging techniques to test the hypothesis that RA patients have more inflammatory, unstable atherosclerotic plaques compared to unaffected individuals and that treatment of active arthritis would lead to alterations in plaque composition and inflammation. Secondary aims were to evaluate the association of clinical phenotype and potential serological biomarkers of CV risk with plaque presence and phenotype. Methods: A prospective pilot study of patients with active RA and age and sex matched controls was conducted. Subjects underwent clinical and serological evaluation, then carotid artery ultrasound was performed to screen for carotid plaque. Dynamic contrast enhanced magnetic resonance imaging (DCE-MRI) was performed on those with suitable plaque. A subgroup of patients had a carotid artery positron emission tomography (PET) scan. Patients were followed up with repeat clinical, serological and DCE-MRI assessments. The primary outcome evaluated was difference in plaque inflammation measured on DCE-MRI between patients and controls and in patients longitudinally. Secondary outcomes included differences in plaque composition on DCE-MRI, plaque inflammation on PET and the relationship of clinical, serological and imaging findings. Results: 130 patients and 52 controls were recruited and screened for carotid plaque. There was a higher prevalence of plaque on ultrasound in the patient group (53% vs 36%) and plaque was independently associated with high sensitivity c reactive protein (hsCRP). Carotid DCE- MRI data was analysed in 15 patients and 5 controls. There was no significant difference in plaque inflammation on DCE-MRI between the groups. However there was a significantly higher rate of plaque calcification in patients, despite similar plaque burden in both groups (73.3% vs 20%, p=0.038). All 15 patients exhibited features of high-risk plaque. Plaque inflammation was seen in all 13 patients in whom PET imaging was undertaken. No significant improvement in plaque inflammation was detected on DCE-MRI over time, which was in keeping with the lack of clinical improvement found in most cases. ConclusionsIncreased prevalence of atherosclerosis and differences in plaque phenotype were observed in this study and findings would support the hypothesis that patients have a more high-risk plaque phenotype. The high prevalence of calcified lesions in RA is a novel finding which warrants further investigation. The study was underpowered to detect significant changes in plaque inflammation, measured on DCE-MRI, between the groups and in patients over time. However, this study provides valuable data with which to plan a larger study to investigate the effects of anti-inflammatory therapy on atherosclerosis in RA in the future.