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ID PMID Title PublicationDate abstract
23504380 First-degree relatives of patients with rheumatoid arthritis exhibit high prevalence of jo 2013 Jun OBJECTIVE: The preclinical period of rheumatoid arthritis (RA) is characterized by the presence of autoantibodies such as anticitrullinated protein antibodies (ACPA) and rheumatoid factor (RF). Little is known about the joint symptom profile preceding onset of RA, and whether symptoms are associated with RA autoantibodies. Because first-degree relatives (FDR) of North American Native (NAN) RA probands exhibit multiple risk factors for development of future RA, we investigated the prevalence of joint symptoms in this high-risk population. METHODS: We studied 306 FDR of NAN patients with RA, 323 NAN controls (NC), and 293 white controls (WC) having no family history of autoimmune diseases. Study subjects completed a questionnaire that asked whether they had pain, swelling, or morning stiffness in their hand joints, or in other joints. Serum samples were gathered at the same time and tested for the presence of ACPA, RF, and high-sensitivity C-reactive protein levels. RESULTS: In all cases, FDR were significantly more likely to report experiencing joint symptoms compared to the 2 control groups. FDR also exhibited a significantly higher prevalence of RA autoantibodies than the control groups. There were modest trends for joint symptoms to associate with RA autoantibodies, and individuals who were both ACPA-positive and RF-positive had the highest prevalence of joint symptoms. CONCLUSION: FDR of NAN patients with RA have a higher prevalence of joint symptoms compared to individuals with no family history of autoimmune disease. This finding is only partially explained by a high prevalence of RA autoantibodies in the FDR.
23606703 The risk of atrial fibrillation in patients with rheumatoid arthritis. 2014 Jun BACKGROUND: Prior research suggests an important role of systemic inflammation in pathogenesis of atrial fibrillation (AF). It is well known that rheumatoid arthritis (RA), a chronic, systemic inflammatory disorder, increases the risk of cardiovascular disease (CVD), but little evidence exists whether the risk of AF is increased in RA. METHODS: Using data from a large US commercial insurance plan, we examined the incidence rate (IR) of hospitalisation for AF in patients with RA compared with non-RA. RA patients were identified with ≥2 separate visits coded for RA and ≥1 disease-modifying antirheumatic drug dispensing. The IR of AF in RA patients was also compared with those with osteoarthritis, a chronic non-inflammatory condition. RESULTS: There were 20 852 RA and 104 260 non-RA patients, matched on age, sex and index date. The mean follow-up was 2 years. The IR per 1000 person-years of AF was 4.0 (95% CI 3.4 to 4.7) in RA and 2.8 (95% CI 2.6 to 3.0) in non-RA patients. The IR ratio for AF was 1.4 (95% CI 1.2 to 1.7) in RA compared with non-RA patients. In a multivariable Cox model adjusting for a number of risk factors such as diabetes, CVD, medications and healthcare utilisation, the risk of AF was no longer increased in RA (HR 1.1, 95% CI 0.9 to 1.4) compared with non-RA patients. There was also no difference in the AF risk between RA and osteoarthritis patients. CONCLUSIONS: Our results show no increased risk of AF associated with RA, after adjusting for various comorbidities, medications and healthcare use.
25481553 Small-molecule therapeutics in rheumatoid arthritis: scientific rationale, efficacy and sa 2014 Aug Rheumatoid arthritis (RA) remains a formidable clinical challenge. This is despite remarkable recent advances in our understanding of pathogenesis and the introduction of a variety of novel agents, particularly biologic therapeutics that are potent inhibitors of extracellular immune pathways. Whereas the latter have brought substantial improvements in efficacy and thus outcomes, there remain significant numbers of non- or partial responders to current standard of care. The discovery of key intracellular pathways, particularly kinases that subserve the function of these pivotal cytokine and immune cell receptors implicated in RA pathogenesis, has facilitated the advent of a new phase of RA drug development. Thus, a range of kinase inhibitors has entered clinical trials and one agent has been licenced for use in some regions. Herein we summarise the chequered history of kinase inhibitor development in RA, describing successes and failures alike, and thereafter examine future trends in this exciting field.
25417294 [Lesions of the radio-carpal joint in patients with rheumatoid arthritis and its surgical 2014 Aug Affection of radio-carpal joint is most frequently revealed in patients, suffering rheumatoid arthritis. While the disease progressing in almost 75% of patients the inflammatory changes in radio-carpal joint occur. An acute and chronic synovitis, damage of a cartilage constitute a cause of a typical erosion of bones inside a joint, weakening of a tendo-ligamentous apparatus and its further deformity. Operative treatment was aimed for the inflammatory focus elimination, reduction of the pain syndrome severity, the function loss, and the joint deformity correction. The mostly used operative interventions are tenoectomy, synovectomy, arthrodesis, total endoprosthesis.
25481550 Stroma: fertile soil for inflammation. 2014 Aug Biological therapies for the management of immune mediated inflammatory diseases such as rheumatoid arthritis have proven to be extremely successful in recent years. Despite these successes, even the most effective of therapies do not lead to cure. Why chronic inflammation persists indefinitely within the rheumatoid synovium despite an absence of continuous stimulation, and why some patients with early synovitis progress to persistent disease whilst others do not, has remained unexplained. In contrast to the paradigm that stromal cells are biochemically active but immunologically passive, there is now growing evidence that stromal components from the rheumatoid synovium play a crucial part in the immunopathology of rheumatoid arthritis. Stromal cells play a central role in the transformation of an acute, resolving to a chronic inflammatory process, and to the persistence of synovial inflammation and joint destruction through a variety of immune mechanisms. Therapeutic manipulation of the stroma is a largely unexplored, yet potentially vital area of research. Targeting pathogenic stromal cells has the potential to provide a cure for chronic inflammatory disorders such as rheumatoid arthritis.
23856797 Lack of association between interleukin-18 polymorphisms and rheumatoid arthritis. 2013 Apr OBJECTIVE: To assess the association of the polymorphisms of the interleukin-18 (IL-18) gene with rheumatoid arthritis (RA) and with risk factors for cardiovascular diseases (CVD). METHODS: This sample comprised 97 patients with RA and 151 healthy controls. In the patients, risk factors for CVD were analyzed, such as cholesterol levels, arterial hypertension, smoking habit, C-reactive protein (CRP) level, and rheumatoid factor. DNA was extracted and the single nucleotide polymorphisms (SNP) at the -607C/A and -137G/C positions of the IL-18 gene were assessed in both groups. The Hardy-Weinberg equilibrium (HWE) was calculated and the odds ratio (OR) test performed, considering a 95% CI and P < 0.05. RESULTS: The frequencies of the -607A allele in patients with RA and in controls were 0,443 and 0.424, respectively, and of the -137C allele, 0.304 and 0.291, respectively. The genotype frequencies were in HWE, except for controls in the -137 locus (P = 0.006). Association of the polymorphisms of the IL-18 gene was found with neither RA nor risk factors for CVD, including cholesterol level and CRP (P > 0.05). In addition, more smokers were found among patients with RA as compared with controls (OR = 1.691; P = 0.088), and the CRP levels were slightly higher in patients who smoked than in patients who did not (OR = 2.673; P = 0.061). CONCLUSIONS: In this sample of patients with RA in the South of Brazil, association of the polymorphisms of the IL-18 gene was observed with neither RA nor risk factors for CVD.
24056520 Neutrophils produce interleukin-17B in rheumatoid synovial tissue. 2014 Jan OBJECTIVE: T helper 17 (Th17) and mast cells produce IL-17A in RA and critically contribute to the pathogenesis of RA. However, the complete IL-17 cytokine profile in RA is unknown. The aim of the study was to systematically study the expression of IL-17 family cytokines in RA. METHODS: The expression of all IL-17 cytokines in RA synovium and pannus as well as in the synovium of OA was determined using quantitative RT-PCR (qRT-PCR). IL-17A and IL-17B were immunostained. Peripheral blood neutrophils were analysed for IL-17B. The effect of IL-17B alone or in combination with TNF-α was tested in vitro on fibroblasts and endothelial cells. RESULTS: In all tissues IL-17B was the most expressed IL-17 family cytokine, found in lining but most strongly expressed in human neutrophil elastase containing polymorphonuclear cells. This pattern was distinct from that of IL-17A, which was found in mast cell tryptase immunoreactive cells. Circulating neutrophils contained IL-17B, verifying the in vivo results. Fibroblasts up-regulated the expression of IL-17RB, a putative receptor of IL-17B, after TNF-α stimulation. IL-17B significantly enhanced TNF-α-induced production of G-CSF and IL-6 in fibroblasts. CONCLUSION: IL-17B, which is present in synovium, may contribute to the pathogenesis of RA. IL-17B can enhance the effects of TNF-α on the production of cytokines and chemokines that control immune cell trafficking and neutrophil homeostasis in the inflamed tissues.
23576073 Biventricular thrombus and associated myocardial infarction in a rheumatoid arthritis pati 2013 Jun Autoimmune diseases including rheumatoid arthritis have an increased incidence of cardiovascular disease. Rheumatoid arthritis (RA) confers a prothrombotic state and is associated with venous thrombosis, but its association with arterial thrombosis and embolism is not clear. In present report, we introduce a unique case of a 42-year-old woman with RA, who was admitted to the emergency service with back pain and diagnosed as having large right and left ventricular thrombus and myocardial infarction, associated with embolization of the thrombus. We also review the literature about RA and arterial and intraventricular thrombosis.
22915624 Impact of intravenous abatacept on synovitis, osteitis and structural damage in patients w 2013 Aug OBJECTIVES: This randomised, double-blind, placebo-controlled phase IIIb study evaluated the impact of abatacept on MRI pathology as a primary outcome in methotrexate (MTX)-refractory patients with rheumatoid arthritis. METHODS: Patients received intravenous abatacept (∼10 mg/kg) or placebo, on background MTX, for 4 months, followed by an 8-month open-label extension (OLE; all patients received abatacept plus MTX). Patients had 1.5T MRI with intravenous contrast at baseline, Months 4 and 12; wrist synovitis (three locations assessed), and wrist and hand (15 and eight locations assessed, respectively) osteitis and erosion were scored using OMERACT-RAMRIS. RESULTS: 26/27 abatacept- and 23/23 placebo-randomised patients completed Month 4 and entered the OLE; 26 and 21 completed Month 12. The primary endpoint was not achieved; mean change (SD) from baseline in synovitis was -0.44 (1.47) for abatacept versus 0.52 (1.38) for placebo (p=0.103) at Month 4. For mean change in synovitis adjusted for baseline score (sensitivity analysis), the difference between groups was -0.69, p=0.078. Adjusted mean changes (SE) in osteitis and erosion were -1.94 (0.86) and 0.45 (0.43) for abatacept, and 1.54 (0.90) and 0.95 (0.45) for placebo. Further MRI improvements were observed up to Month 12 for abatacept and from Months 4 to 12 for placebo-treated patients switched to abatacept at Month 4. Clinical efficacy was shown with abatacept and sustained to Month 12. CONCLUSIONS: Despite small patient numbers, MRI detected structural and synovial benefit, sustained to Month 12 in abatacept+MTX-treated patients, and improvements in structural and inflammatory outcomes for placebo+MTX-treated patients following addition of abatacept. CLINICAL TRIAL REGISTRATION: Clinicaltrials.gov NCT00420199.
23992372 Rheumatoid arthritis is caused by a Proteus urinary tract infection. 2014 May Genetic, molecular and biological studies indicate that rheumatoid arthritis (RA), a severe arthritic disorder affecting approximately 1% of the population in developed countries, is caused by an upper urinary tract infection by the microbe, Proteus mirabilis. Elevated levels of specific antibodies against Proteus bacteria have been reported from 16 different countries. The pathogenetic mechanism involves six stages triggered by cross-reactive autoantibodies evoked by Proteus infection. The causative amino acid sequences of Proteus namely, ESRRAL and IRRET, contain arginine doublets which can be acted upon by peptidyl arginine deiminase thereby explaining the early appearance of anti-citrullinated protein antibodies in patients with RA. Consequently, RA patients should be treated early with anti-Proteus antibiotics as well as biological agents to avoid irreversible joint damages.
23588941 Prognostic factors and radiographic outcomes of nontuberculous mycobacterial lung disease 2013 Aug OBJECTIVE: The aims of our study were to retrospectively review patients with rheumatoid arthritis (RA) with nontuberculous mycobacterial (NTM) lung disease, to assess the prognostic factors, and to analyze the time to disease deterioration according to the antirheumatic drugs received during the NTM lung disease followup period. METHODS: We retrospectively analyzed medical records of 98 HIV-negative RA patients with NTM lung disease treated at our institution, and investigated potential risk factors of mortality with Cox regression analysis. Time to radiologic deterioration was evaluated if antirheumatic drugs were not changed during observational periods and computed tomography was performed once each year. RESULTS: Mean patient age was 67.6 years, and median followup period was 4.4 years. NTM species included Mycobacterium avium complex (83.7%), M. kansasii (6.1%), M. gordonae (6.1%), and others (4.1%). Radiographic features included nodular/bronchiectatic (NB) disease (57.1%), fibrocavitary (FC) disease (14.3%), FC+NB disease (16.3%), and other types (12.2%). Initial management included observation in 74 (75.5%) patients. Negative prognostic factors of mortality were C-reactive protein (CRP) ≥ 1.0 mg/dl and radiographic features of FC, FC+NB, or other disease types. Median time to radiologic deterioration was 3.6 years. Erythrocyte sedimentation rate (ESR) > 50 mm/h was a negative prognostic factor of radiologic deterioration. CONCLUSION: The most frequent NTM species was M. avium complex. CRP and radiographic features were prognostic factors for all-cause mortality, and ESR was a prognostic factor of radiologic deterioration. Further studies are warranted focusing on time to disease deterioration according to antirheumatic drug received during NTM followup.
23255070 Synovitis and bone inflammation in early rheumatoid arthritis: high-resolution multi-pinho 2013 Jan PURPOSE: We aimed to assess the relationship between bone inflammation in multi-pinhole single-photon emission computed tomography (MPH-SPECT) and synovitis detected by magnetic resonance imaging (MRI) in early rheumatoid arthritis patients. MATERIALS AND METHODS: MPH-SPECT with technetium dicarboxypropanedisphosphonate (Tc-99mDPD) and 3 Tesla MRI were performed in 10 early rheumatoid arthritis patients. Eighty finger joint sites were assessed for increased osteoblastic activity using visual and region-of-interest (ROI) analysis. Presence of joint inflammation in MRI was investigated using the subscores of the rheumatoid arthritis MRI score. RESULTS: Tc-99mDPD uptake was increased in 38 (47.5%) and 22 (27.5%) joint sites as determined by visual and ROI analysis, respectively. A total of 32 (84.2%) sites with increased bone metabolism showed a normal MRI bone signal. The MPH-SPECT uptake ratio was elevated only in the subgroup with severe synovitis (P < 0.001). CONCLUSION: In early rheumatoid arthritis, molecular imaging with MPH-SPECT detects higher rates of inflammatory bone involvement compared to MRI. Our preliminary data suggest that osteitis is related to severe synovitis.
24252044 Long-term clinical and radiographic results of cementless total hip arthroplasty for patie 2014 Mar OBJECTIVES: The aim of this study was to clarify the long-term clinical and radiographic results of cementless total hip arthroplasty (THA) for patients with rheumatoid arthritis (RA). METHODS: Twenty-eight total hip arthroplasties in 24 patients with a diagnosis of RA were performed from October 1992 to October 1996. All components were titanium alloy with a circumferential porous coating. Six patients (six hips) died before the 10-year follow-up, and one patient (one hip) was lost to follow-up, leaving 21 joints of 17 patients for review at a minimum 10-year follow-up after surgery. There were 3 men and 14 women with an average age of 55.0 years. The average duration of RA at the time of the operation was 12.6 years, and the average follow-up period was 12.2 years. We evaluated the Japanese Orthopaedic Association (JOA) hip scores, radiographic changes and survivor rates of components. RESULTS: Compared with the preoperative JOA hip scores, there was significant improvement in the postoperative scores. Spot welds consistent with bone ingrowth were identified in 95.0% of the femoral components. No femoral components showed radiographic loosening or required revision for aseptic loosening, but two acetabular revisions were performed because of aseptic loosening. The 14-year survivor rates of the stem and cup with the end point of loosening were 100% and 88.2%, respectively. CONCLUSIONS: Cementless THA with this component design in patients with RA appears to be a promising treatment.
22802010 Ultrasonography is a potent tool for the prediction of progressive joint destruction durin 2013 May OBJECTIVES: Although "clinical remission" has been a realistic goal of treatment in rheumatoid arthritis (RA), there is evidence that subclinical synovitis is associated with ongoing structural damage even after clinical remission is achieved. In the study reported here, we assessed whether ultrasonography (US) can predict progressive joint destruction during clinical remission of RA. METHODS: Thirty-one patients with RA in clinical remission based on the disease activity score in 28 joints were recruited for this study. Bilateral wrists and all of the metacarpophalangeal and proximal interphalangeal (PIP) joints were examined by power Doppler (PD) ultrasonography (US), and the PD signals were scored semiquantitatively in each joint. The total PD score was calculated as the sum of individual scores for each joint. RESULTS: Among 22 RA patients who maintained clinical remission during the 2-year follow-up period, seven showed radiographic progression. Radiographic progression was strongly associated with total PD score at entry, with all patients showing radiographic progression having a total PD score of ≥ 2 at entry and none of the patients with a total PD score of ≤ 1 showing any radiographic progression. There was no significant association of therapeutic agents with progressing or non-progressing cases. CONCLUSIONS: PD-US detects synovitis causing joint destruction even when the patient is in clinical remission. Thus, remission visible on US is essential to reach "true remission" of RA.
23649045 The role of miR-155 in regulatory T cells and rheumatoid arthritis. 2013 Jul Recently, various micro(mi)RNAs have been found deregulated in the setting of rheumatoid arthritis (RA), but their role in the pathogenesis of this disease remains a matter of debate. In the meanwhile, increasing evidence indicates a defective function of regulatory T cells (Tregs) in RA. This review discusses relevant studies addressing the function of Tregs and Cytotoxic T-Lymphocyte Antigen 4 in RA, provides recent data on the role of miRNAs for Tregs homeostasis, and focuses on the role of miR-155 in Tregs. In a final perspective section we discuss the potential impact of therapeutic miR-155 modulation in RA.
23897768 Association of circulating miR-223 and miR-16 with disease activity in patients with early 2014 Oct BACKGROUND: Identification of parameters for early diagnosis and treatment response would be beneficial for patients with early rheumatoid arthritis (ERA) to prevent ongoing joint damage. miRNAs have features of potential biomarkers, and an altered expression of miRNAs was shown in established rheumatoid arthritis (RA). OBJECTIVE: To analyse RA associated miRNAs in the sera of patients with ERA to find markers of early disease, clinical activity or predictors of disease outcome. METHODS: Total RNA was isolated from whole sera in ERA patients (prior to and after 3 and 12 months of therapy with disease modifying antirheumatic drugs), in patients with established RA and in healthy controls (HC) using phenol-chloroform extraction. Expression of miR-146a, miR-155, miR-223, miR-16, miR-203, miR-132 and miR-124a was analysed by TaqMan Real Time PCR. RESULTS: From all analysed miRNAs, levels of miR-146a, miR-155 and miR-16 were decreased in the sera of ERA patients in comparison with established RA. A change in circulating miR-16 in the first 3 months of therapy was associated with a decrease in DAS28 in long term follow-up in ERA (p=0.002). Levels of circulating miR-223 in treatment naïve ERA correlated with C reactive protein (p=0.008), DAS28 (p=0.031) and change in DAS28 after 3 months (p=0.003) and 12 months (p=0.011) of follow-up. However, neither miR-16 nor miR-223 could distinguish ERA from HC. CONCLUSIONS: Differential expression of circulating miR-146a, miR-155 and miR-16 in the sera of ERA patients may characterise an early stage of the disease. We suggest miR-223 as a marker of disease activity and miR-16 and miR-223 as possible predictors for disease outcome in ERA.
22198659 Serum ghrelin in female patients with rheumatoid arthritis during treatment with inflixima 2013 Jun Ghrelin is a gastric hormone that posses multiple functions, including induction of growth hormone release, regulation of proinflammatory cytokines and control of food intake and energy homeostasis. A few reports on serum ghrelin level in chronic inflammatory states revealed contradictory results. The study was undertaken to determine ghrelin in patients with rheumatoid arthritis receiving infliximab, a TNF-α blocking agent. Serum ghrelin was determined in 18 female rheumatoid patients before the treatment with infliximab, 1 week after the first infusion and after 53 weeks of medication and compared with 15 age-matched healthy women. Serum ghrelin level was shown to be increased in the patients. A decrease in serum ghrelin level was found after the first infusion of infliximab and similarly decreased ghrelin level but still higher than in the control was shown in the 53rd week of medication. The obtained results suggest that ghrelin level is related to inflammation, and its serum level in patients with severe rheumatoid arthritis behaves similarly to acute-phase reactants.
24513290 Aberrant histone acetylation contributes to elevated interleukin-6 production in rheumatoi 2014 Feb 21 Accumulating evidence indicates that epigenetic aberrations have a role in the pathogenesis of rheumatoid arthritis (RA). However, reports on histone modifications are as yet quite limited in RA. Interleukin (IL)-6 is an inflammatory cytokine which is known to be involved in the pathogenesis of RA. Here we report the role of histone modifications in elevated IL-6 production in RA synovial fibroblasts (SFs). The level of histone H3 acetylation (H3ac) in the IL-6 promoter was significantly higher in RASFs than osteoarthritis (OA) SFs. This suggests that chromatin structure is in an open or loose state in the IL-6 promoter in RASFs. Furthermore, curcumin, a histone acetyltransferase (HAT) inhibitor, significantly reduced the level of H3ac in the IL-6 promoter, as well as IL-6 mRNA expression and IL-6 protein secretion by RASFs. Taken together, it is suggested that hyperacetylation of histone H3 in the IL-6 promoter induces the increase in IL-6 production by RASFs and thereby participates in the pathogenesis of RA.
25194942 Characterization and quantification of angiogenesis in rheumatoid arthritis in a mouse mod 2014 Sep 6 BACKGROUND: Angiogenesis is an important pathophysiological process of chronic inflammation, especially in inflammatory arthritis. Quantitative measurement of changes in vascularization may improve the diagnosis and monitoring of arthritis. The aim of this work is the development of a 3D imaging and analysis framework for quantification of vascularization in experimental arthritis. METHODS: High-resolution micro-computed tomography (μCT) was used to scan knee joints of arthritic human tumor necrosis factor transgenic (hTNFtg) mice and non-arthritic wild-type controls previously perfused with lead-containing contrast agent Microfil MV-122. Vessel segmentation was performed by combination of intensity-based (local adaptive thresholding) and form-based (multi-scale method) segmentation techniques. Four anatomically defined concentric spherical shells centered in the knee joint were used as analysis volumes of interest. Vessel density, density distribution as well as vessel thickness, surface, spacing and number were measured. Simulated digital vessel tree models were used for validation of the algorithms. RESULTS: High-resolution μCT allows the quantitative assessment of the vascular tree in the knee joint during arthritis. Segmentation and analysis were highly automated but occasionally required manual corrections of the vessel segmentation close to the bone surfaces. Vascularization was significantly increased in arthritic hTNFtg mice compared to wild type controls. Precision errors for the morphologic parameters were smaller than 3% and 6% for intra- and interoperator analysis, respectively. Accuracy errors for vessel thickness were around 20% for vessels larger than twice the resolution of the scanner. CONCLUSIONS: Arthritis-induced changes of the vascular tree, including detailed and quantitative description of the number of vessel branches, length of vessel segments and the bifurcation angle, can be detected by contrast-enhanced high-resolution μCT.
23441768 Cardiovascular morbidity in rheumatoid arthritis patients in North Canterbury, New Zealand 2013 Feb AIM: Cardiovascular disease is a substantial contributor to increased morbidity and mortality in rheumatoid arthritis (RA). The aim of this audit was to determine the rate of cardiovascular events in a cohort of newly diagnosed RA patients. METHOD: The inpatient clinical database from Christchurch Hospital, Christchurch, New Zealand, was searched using the International Classification of Diseases 9th Revision (ICD9) and 10 codes representing RA and cardiovascular disease between 1 January 1999 and 31 December 2008. Notes were reviewed with additional demographic and medication data sought. Outpatient data for RA patients was collated from the Rheumatology Department's letter database. RESULTS: Four hundred and six patients were identified with combined ICD9 or 10 codes for RA and ischemic heart disease, of whom 194 had a confirmed myocardial event. Of these, 34 were diagnosed with RA between January 1999 and December 2008 prior to their myocardial event. Kaplan-Meier analysis showed risk of a cardiovascular event at 1 and 10 years was 0.64% and 9.4%, respectively. There were 26 confirmed deaths in the study period. The risk of death at 1 and 10 years was 0.48% and 8.16%, respectively. CONCLUSION: We have shown a relatively low prevalence of cardiovascular events in this RA population diagnosed within a 10 year period. This is consistent with other reports and likely reflects the short follow-up period. Prospective longer-term studies will be required to further investigate the relative contribution of disease activity and other parameters to cardiovascular events in patients with early RA.