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Search for: rheumatoid arthritis    methotrexate    autoimmune disease    biomarker    gene expression    GWAS    HLA genes    non-HLA genes   

ID PMID Title PublicationDate abstract
15290729 Serum galactosyltransferase isoform changes in rheumatoid arthritis. 2004 Aug OBJECTIVE: To investigate glycosylation changes associated with rheumatoid arthritis (RA) by determining whether there are beta1,4-galactosyltransferase (GTase) isoforms specific to or altered in the serum of patients with RA. Methods. Serum GTase isoform profiles were determined using isoelectric focusing (IEF) in patients with active RA (n = 9), disease controls (DC; n = 9), and healthy individuals (HI; n = 10). RESULTS: There was a highly significant difference (p < 0.0001) between the IEF profiles. The RA IEF profile was significantly (p < 0.0001) different from that of the DC or the HI group. There was, however, no significant difference between the DC and HI profiles. Serum GTase samples from 8/9 RA, 9/9 DC, and 9/10 HI resolved into 2 distinct peaks of activity. The RA isoform profile was associated with an acidic shift. There were no significant differences in the pH value of the first peak; the second peak was found to be significantly more acidic in the RA group (mean pH 5.02) compared to the DC and HI group (mean pH 5.20; p < 0.05). The RA associated isoform constituted a significantly greater proportion of total enzymatic activity in the RA sera (16.1%) compared to DC and HI (13.5%; p < 0.05 and 12.6%; p < 0.01, respectively). RA and HI serum GTase desialylation resulted in an alkaline shift of the isoforms into similar pH bands: 5.25-5.50, 5.70-5.85, and 6.20-6.40. GTase was found to be on average 75% more active in its desialylated form than in its sialylated state. CONCLUSION: RA is associated with a differential expression of GTase isoforms. This may be due to increased hypersialylation, which has the potential to adversely affect the catalytic activity of the enzyme, thus providing a possible mechanism for posttranslational regulation of GTase activity in RA.
15476247 Severity of murine collagen-induced arthritis correlates with increased CYP7B activity: en 2004 Oct OBJECTIVE: The endogenous steroid dehydroepiandrosterone (DHEA) has been reported to play a role in rheumatoid arthritis (RA). DHEA is metabolized by the P450 enzyme CYP7B into 7alpha-OH-DHEA, which has immunostimulating properties. This study was undertaken to investigate the putative role of CYP7B in arthritis using murine collagen-induced arthritis (CIA), an interleukin-1beta (IL-1beta)-dependent model. METHODS: DBA/1J mice were immunized and administered a booster with type II collagen. The presence of 7alpha-OH-DHEA was determined in both arthritic and nonarthritic joints and the serum of CIA mice by radioimmunoassay. CYP7B messenger RNA (mRNA) expression was analyzed in synovial biopsy samples, and in fibroblast-like synoviocytes (FLS) isolated from these synovial biopsy samples, by reverse transcriptase-polymerase chain reaction (RT-PCR). In addition, the regulatory role of IL-1beta on CYP7B activity in FLS was determined using RT-PCR, Western blotting, and high-performance liquid chromatography. RESULTS: In knee joint synovial biopsy samples from arthritic mice, 7alpha-OH-DHEA levels were 5-fold higher than in nonarthritic mice. Elevated levels of 7alpha-OH-DHEA were accompanied by an increase in CYP7B mRNA expression and were positively correlated with disease severity. In serum, no differences in 7alpha-OH-DHEA levels were observed between arthritic and nonarthritic mice. Incubation of FLS with IL-1beta resulted in a dose-dependent increase in 7alpha-OH-DHEA formation. In addition, IL-1beta enhanced CYP7B mRNA and CYP7B protein levels in FLS. CONCLUSION: Disease progression in CIA is correlated with enhanced CYP7B activity, which leads to locally enhanced 7alpha-OH-DHEA levels. Elevated IL-1beta levels within the arthritic joint may regulate this increase in CYP7B activity.
12495361 Benefit-risk assessment of infliximab in the treatment of rheumatoid arthritis. 2003 In the last decade, there have been substantial advances in the treatment of rheumatoid arthritis with the addition of several new disease-modifying agents to the therapeutic armamentarium. Biological agents targeting tumour necrosis factor (TNF) represent one such important addition. Infliximab, a chimeric anti-TNF monoclonal antibody, has shown remarkable promise in alleviating the signs and symptoms of rheumatoid arthritis in addition to retarding radiographic disease progression when used in combination with methotrexate. In its pivotal phase III trial, the addition of infliximab to patients with methotrexate-refractory disease was associated with substantial clinical benefit. Using American College of Rheumatology criteria for improvement, one-half of patients receiving infliximab (3 mg/kg every 8 weeks) plus methotrexate showed at least 20% improvement compared with only 20% of those receiving placebo plus methotrexate (p < 0.001) with over one-half of eventual responders obtaining criteria for improvement by the second week of observation. Although its use has been met with much deserved enthusiasm, recent reports have highlighted several potential serious adverse effects associated with infliximab (and other TNF antagonists), including infusion reactions, congestive heart failure, drug-induced lupus, and CNS demyelination. In addition, recent reports have cited the potential for reactivation of mycobacterial and fungal infection in patients receiving infliximab, mandating appropriate tuberculosis screening prior to drug initiation. Although the frequency of serious drug-related toxicity (requiring discontinuation of the agent) appears to be quite low, these reports underscore the need for caution and close surveillance with the administration of TNF inhibitors, particularly given that strategies aimed at preventing toxicity remain unproven. Despite its potential for toxicity, infliximab remains a valuable alternative for patients with rheumatoid arthritis.
15123038 The transfer of a laboratory based hypothesis to a clinically useful therapy: the developm 2004 Feb The development of anti-TNF therapy is a key step forward in rheumatology as it is the first new therapy for based on investigating the molecular mechanisms of this disease. This chapter reviews how this discovery was made.
12794815 Etanercept added to background methotrexate therapy in patients with rheumatoid arthritis: 2003 Jun OBJECTIVE: To observe the long-term safety and efficacy of combination therapy with etanercept and methotrexate in patients with rheumatoid arthritis (RA), and to determine whether the addition of etanercept allowed reductions in methotrexate or corticosteroid dosages while maintaining a clinical response. METHODS: Patients with RA who received methotrexate plus etanercept in a previous randomized, placebo-controlled trial were offered the opportunity to enroll in an open-label extension study for further evaluation of treatment with etanercept and methotrexate. RESULTS: Seventy-nine of the 89 patients in the original blinded study enrolled in the extension study, and 65 of these patients continue in the study. Patients have received etanercept therapy for up to 47 months (median 44 months). The types and rate of adverse events noted during the extension trial were similar to those observed in the controlled trial. At the 3-year assessment, 77% of the 57 patients available for evaluation met American College of Rheumatology 20% (ACR20) criteria for improvement in RA, 47% met the ACR50 criteria, and 23% met the ACR70 criteria. Of the 36 patients assessed at 3 years in the extension study, 30 (83%) were able to decrease their dosages of corticosteroids, and 20 (56%) were able to discontinue corticosteroid therapy. At 3 years, the dosage of methotrexate was decreased in 41 of 66 patients (62%), and methotrexate therapy was discontinued in 19 patients (29%). CONCLUSION: In this observational continuation study, the addition of etanercept to background methotrexate provided sustained clinical benefit over a median period of 44 months. With etanercept therapy, there were trends toward dosage reduction or discontinuation of methotrexate and corticosteroids, without apparent worsening of ACR response rates. Compared with the controlled trial, no increases in the rate of adverse events were observed.
12847672 Five-year followup of rheumatoid arthritis patients after early treatment with disease-mod 2003 Jul OBJECTIVE: To evaluate whether the clinical advantages observed after 1 year in a randomized controlled clinical trial, in which 2 treatment strategies were compared (the early disease-modifying antirheumatic drug [DMARD] approach versus the pyramid approach), persist after 5 years. METHODS: In this study, 238 patients with recently diagnosed rheumatoid arthritis (RA) were randomized to either the pyramid group (n = 56) or the early DMARD group (n = 182). Patients assigned to the pyramid group received nonsteroidal antiinflammatory drugs for at least 1 year after inclusion (the mean +/- SD lag time until first prescription of a DMARD was 14 +/- 9 months). Patients in the early DMARD group were treated with a DMARD immediately after inclusion. RESULTS: After 5 years, data were available for 44 patients in the pyramid group (79%) and 145 patients in the early DMARD group (80%). No prolongation of the clinical advantages in favor of the early DMARD group, as observed after the first year, was demonstrated. Nevertheless, a significantly shorter delay time until complete response and a higher number of patients with overall clinically relevant improvement at several assessment points were observed in the early DMARD group compared with the pyramid group. CONCLUSION: The clinical results in favor of the early DMARD group, as observed after the first year, were not as evident after 5 years. This indicates that a more aggressive treatment approach in early RA is required, and that treatment should be continued for a prolonged period of time, in order to maintain the advantages obtained in the first year.
12707361 Albumin-based drug delivery as novel therapeutic approach for rheumatoid arthritis. 2003 May 1 We reported recently that albumin is a suitable drug carrier for targeted delivery of methotrexate (MTX) to tumors. Due to pathophysiological conditions in neoplastic tissue, high amounts of albumin accumulate in tumors and are metabolized by malignant cells. MTX, covalently coupled to human serum albumin (MTX-HSA) for cancer treatment, is currently being evaluated in phase II clinical trials. Because synovium of patients with rheumatoid arthritis (RA) shares various features observed also in tumors, albumin-based drug targeting of inflamed joints might be an attractive therapeutic approach. Therefore, the pharmacokinetics of albumin and MTX in a mouse model of arthritis was examined. Additionally, uptake of albumin by synovial fibroblasts of RA patients and the efficacy of MTX and MTX-HSA in arthritic mice were studied. The results show that when compared with MTX, significantly higher amounts of albumin accumulate in inflamed paws, and significantly lower amounts of albumin are found in the liver and the kidneys. The protein is metabolized by human synovial fibroblasts in vitro and in vivo. MTX-HSA was significantly more effective in suppression of the onset of arthritis in mice than was MTX. In conclusion, albumin appears to be a suitable drug carrier in RA, most likely due to effects on synovial fibroblasts, which might increase therapeutic efficacy and reduce side effects of MTX.
12732875 Gene therapy for arthritis. 2003 May Rheumatoid arthritis is an autoimmune disease with intra-articular inflammation and synovial hyperplasia that results in progressive degradation of cartilage and bone, in severe cases it causes systemic complications. Recently, biological agents that suppress the activities of proinflammatory cytokines have shown efficacy as antiarthritic drugs, but require frequent administration. Thus, gene transfer approaches are being developed as an alternative approach for targeted, more efficient and sustained delivery of inhibitors of inflammatory cytokines as well as other therapeutic agents. Indeed, the efficacy of gene transfer for the treatment of arthritis has been demonstrated in mouse, rat, rabbit, and horse models of disease whereas the feasibility of the approach has been demonstrated in Phase I clinical trials. In this review, the current status of both preclinical and clinical arthritis gene therapy is presented. In addition, the advantages and disadvantages of different types of vectors, target cells and therapeutic genes being developed for the treatment of arthritis are summarized. Finally, the future directions of the rapidly developed field of arthritis gene therapy are outlined.
14993719 Arthritis in lymphomatoid granulomatosis: report of a case and review of literature. 2004 Feb Lymphomatoid granulomatosis (LG) is a rare systemic vasculitis caused by Epstein Barr virus induced transformation of the B-cells in a T-cell rich environment. The predominant clinical presentations are confined to the pulmonary system however; extra-pulmonary manifestations can sometimes be the main feature of the disease. Here in we describe a 52-year-old female who presented with symmetric polyarthritis and generalized stiffness for 7 months and papular lesions over extremities for 3 months duration. She in addition had generalized lymphadenopathy. Histopathological examination of the cutaneous lesions confirmed LG. Patient died despite therapy with cyclophosphamide and prednisolone. This is the first report of LG mimicking rheumatoid arthritis from India.
15027483 Anti-TNFalpha therapy of rheumatoid arthritis: what can we learn about chronic disease? 2004 The importance of tumour necrosis factor (TNF)alpha in rheumatoid arthritis (RA) was initially proposed on the basis of analysis of cytokine gene regulation at the local site of the disease, the synovium. This was then verified in animal models and established in an extensive series of clinical trials, culminating in now 250000 treated patients with either of two approved TNF inhibitors, antibody or fusion protein. The degree and magnitude of clinical benefit has enabled analyses of the mechanism by which anti-TNF benefits, and hence insights into important steps in the disease process. It was found that essentially all aspects of RA were ameliorated, and important mechanisms of benefit involved diminution of multiple pro-inflammatory cytokines, adhesion molecules and chemokines, leading to reduced cell trafficking, reduced angiogenesis and most importantly halting of joint destruction. What of the problems? Safety is better than prior drugs, but there is a small increase in severe infections, smaller than might have been anticipated. Cost is the major drawback limiting greater use. In view of the central pathological processes down-regulated, and their role in many diseases, the early clinical success of anti-TNF in RA led to subsequent successful trials and registration in Crohn's disease and juvenile rheumatoid arthritis, and successful trials in ankylosing spondylitis, psoriasis and psoriatic arthritis. The era of anti-cytokine therapeutics is just dawning.
15476203 Association of increased expression of macrophage elastase (matrix metalloproteinase 12) w 2004 Oct OBJECTIVE: Increased enzymatic activity of matrix metalloproteinases (MMPs) may promote the progression of rheumatoid arthritis (RA). We undertook this study to investigate the expression and localization of human macrophage elastase (MMP-12) in synovial tissue from RA patients and to compare MMP-12 levels in the synovial tissue and synovial fluid of RA patients with the corresponding levels in patients with osteoarthritis (OA). METHODS: We obtained synovial tissues from 23 RA patients and 29 OA patients and analyzed MMP-12 expression using immunohistochemistry, Western and Northern blotting analyses, and zymography. Furthermore, we quantified MMP-12 levels in synovial fluid by Western blotting and zymography. RESULTS: Northern blotting analysis demonstrated that RA synovial tissue contained higher levels of MMP-12 messenger RNA than did OA synovial tissue. Western blotting revealed that MMP-12 proteins were consistently and markedly increased in RA synovial tissue compared with OA synovial tissue. A greater amount of immunoreactive proteins corresponding to catalytic forms of MMP-12 was present in RA synovial tissue and synovial fluid, and the MMP-12 proteins exhibited caseinolytic activity in vitro. Immunohistochemical staining showed that the major cells expressing MMP-12 were synovial lining cells, many of which were inflammatory macrophages. CONCLUSION: These results establish a possible mechanism by which macrophage-derived MMP-12 may play an important role in the destructive process in RA. Inhibition of MMP-12 may be a potential modality for the treatment of RA.
12687539 High mobility group box chromosomal protein 1 plays a role in the pathogenesis of rheumato 2003 Apr OBJECTIVE: High mobility group box chromosomal protein 1 (HMGB-1), a nuclear DNA binding protein, was recently rediscovered as a new proinflammatory cytokine. The purpose of this study was to demonstrate HMGB-1 expression in vivo and to identify the role of HMGB-1 in the pathogenesis of rheumatoid arthritis (RA). METHODS: HMGB-1 concentrations in synovial fluid (SF) and serum from RA and osteoarthritis (OA) patients were measured by immunoblot analysis. The protein's specific receptor, receptor for advanced glycation end products (RAGE), was examined in SF macrophages (SFMs). We measured levels of proinflammatory cytokines released by SFMs treated with HMGB-1 via enzyme-linked immunosorbent assay and used soluble RAGE (sRAGE) to block the release of tumor necrosis factor alpha (TNFalpha). Immunohistochemical analysis and immunofluorescence assay were employed to examine localization of HMGB-1 in RA synovium and its translocation in SFMs after TNFalpha stimulation. RESULTS: HMGB-1 concentrations were significantly higher in SF of RA patients than in that of OA patients. SFMs expressed RAGE and released TNFalpha, interleukin-1beta (IL-1beta), and IL-6 upon stimulation with HMGB-1. HMGB-1 was found in CD68-positive cells of RA synovium, and TNFalpha stimulation translocated HMGB-1 from the nucleus to the cytosol in SFMs. Blockade by sRAGE inhibited the release of TNFalpha from SFMs. CONCLUSION: HMGB-1 was more strongly expressed in SF of RA patients than in that of OA patients, inducing the release of proinflammatory cytokines from SFMs. HMGB-1 plays a pivotal role in the pathogenesis of RA and may be an original target of therapy as a novel cytokine.
15686185 [TNF alfa modulators in the treatment of rheumatoid arthritis]. 2004 Oct Current slow-acting anti-rheumatic drugs available at now for rheumatoid arthritis fail in majority of cases and have an inconstant chondro-protective effect. Improvements in our knowledge of its pathogenesis and advances in molecular biology have made possible to develop selective immunotherapy approaches. Tumor necrosis factor alfa (TNF alfa) is an important inflammatory mediator that play a crucial role in rheumatoid arthritis. This studies summarizes clinical essays that evaluate beneficial effects and tolerance of anti TNF alfa antibodies. This study showed the clinical, biological and radiological efficacy of these therapeutic agents. But some doubts persist concerning their long term side effects particularly infections, neoplasm or auto immune ones. High price of this treatment should evaluate report cost benefice to appreciate the better utilisation of these drugs.
15151041 [Aortic valve regurgitation associated with rheumatoid arthritis; report of a case]. 2004 May We report a rare case of aortic regurgitation (AR) associated with rheumatic arthritis (RA). A 59-year-old female was brought to our hospital with cardiopulmonary arrest because of severe heart failure due to AR. After being treated for heart failure, aortic valve replacement was carried out with a Carpentier-Edwards 21 mm model. During operation, it was observed that all of the coronary cusps had become thickened and shortened. A part of the right coronary cusp near the commissure of the left coronary cusp was especially badly affected. Valve histology showed a typical degeneration pattern. The patient had an uneventful postoperative course. It appears likely that the aortic valve had become shortened during the recovery process from inflammation caused by RA. The use of bioprostheses is beneficial in RA patients with aortitis, gastric ulcers, etc., since they reduce dynamic stress and eliminate the need for use of anti-coagulants.
12382786 Experimental validation of Monte Carlo depth-dose calculations using radiochromic dye film 2002 In this work we compare the Monte Carlo (MCNP4B) calculated beta-gamma depth-dose profile for a liquid 153Sm beta-gamma source used in radiation synovectomy with the experimental depth-dose distribution obtained using radiochromic dye film dosimetry. The calculated and experimental depth-dose distribution shows a very good agreement (within 5%) in the region where the dose deposition is dominated by the beta particle component (first 800 microm depth on tissue-equivalent material). The agreement worsens, reaching a maximum deviation of 15%, at depths close to the maximum range of the beta particles. Finally the agreement improves for the region where the gamma component accounts for one-third of the total absorbed dose (depths >1 mm). The possible contributions to these differences are discussed, as well as their relevance for the application of 153Sm in the treatment of rheumatoid arthritis.
15080264 Peptidylarginine deiminase, the arginine to citrulline converting enzyme, is frequently re 2003 OBJECTIVE: Antibodies to citrulline-containing epitopes of filaggrin are highly specific for rheumatoid arthritis (RA). We studied whether the enzyme peptidylarginine deiminase (PAD), responsible for the post-translational modification of peptide-bound arginine residues to citrulline, constitutes an antigen for patients with RA. METHODS: IgG antibodies to PAD were measured by enzyme-linked immunosorbent assay (ELISA) in sera from patients with RA, systemic lupus erythematosus (SLE), primary Sjögren syndrome (pSS), multiple sclerosis (MS) and healthy controls. RESULTS: Compared to healthy controls, raised levels of IgG antibodies to PAD were found in 50 of 57 recent-onset RA patients (88%) and in 40 (70%) of the same 57 patients 3 years later (p<0.0001 for both comparisons). Eleven of 51 (22%) patients with RA of long duration, 19/43 (44%) patients with SLE and 16/19 (84%) patients with pSS, but none of 20 patients with MS, had elevated anti-PAD levels. CONCLUSION: The arginine-citrulline converting enzyme PAD was recognized as a new antigen against which patients with inflammatory rheumatic diseases frequently show IgG class antibodies.
15111902 Total elbow arthroplasty with massive composite allografts. 2004 May Total elbow arthroplasty is challenging when there is extensive bone loss. We studied retrospectively the long-term (mean, 6.5 years) clinical and radiographic results of 10 patients in whom 14 massive allograft-prosthetic composites were used in such clinical situations. The mean arc of active flexion/extension was 92 degrees. The Bryan-Morrey and Hospital for Special Surgery elbow scoring systems were used and revealed a modest improvement in pain and stability but a disappointing return of function, with independent self-care possible in only 3 patients, household and employment activities in 2, and recreational pursuits in 2. Three patients claimed that they were unable to use the elbow. Multiple procedures (mean, 2.2) were sometimes required to optimize the result. The 79% rate of allograft-host union is similar to that of hip and knee arthroplasty. The use of massive allografts is a reasonable alternative in salvage situations involving total elbow arthroplasty with massive bone loss.
14978019 The point mutation of tyrosine 759 of the IL-6 family cytokine receptor gp130 synergizes w 2004 Mar Rheumatoid arthritis (RA) is a polygenic autoimmune disease. The autoimmunity develops from synergistic actions of genetic and environmental factors. We generated a double-mutant mouse by crossing two murine models of RA, a gp130 mutant knock-in mouse (gp130F759/F759) and an HTLV-1 pX transgenic mouse (pX-Tg), in a C57BL/6 background, which is resistant to arthritis. The mice spontaneously developed severe arthritis with a much earlier onset than the gp130F759/F759 mice and with a much higher incidence than did the pX-Tg mice. The symptoms of gp130F759/F759 mice, including lymphoadenopathy, splenomegaly, hyper-gamma-globulinemia, autoantibody production, increases in memory/activated T cells and granulocytes in the peripheral lymphoid organs, and a decrease in the class II MHC(bright) CD11c+ population, were augmented in the double mutants. Marked reductions in incidence, severity and immunological abnormalities were seen in the triple mutant, IL-6-/-/gp130F759/F759/pX-Tg, indicating that the arthritis in the double mutant is IL-6 dependent. gp130F759/F759/pX-Tg is a unique mouse model for RA.
15552527 Demyelination and inhibition of tumor necrosis factor (TNF). 2004 Sep The development of tumor necrosis factor alpha (TNFalpha) inhibitor therapy is arguably the most significant achievement in the treatment of rheumatic diseases to date. One serious potential side effect associated with these agents is the onset of neurologic signs and symptoms. In this paper we will examine the relationship of TNFalpha antagonism and demyelinating disease. Reviewing early laboratory and animal models, we discuss the mechanism of TNFalpha in central nervous system (CNS) injury and repair. Two negative studies of TNFa inhibitor therapy in the treatment of refractory multiple sclerosis (MS) are considered. From the manufacturers' clinical development programs and post-marketing adverse event reporting data, we report the current incidence of demyelinating symptoms associated with each of the commercially available anti-TNFa agents. Comparing these reports to the incidence of MS in society as a whole, we find the rate of new cases of neurologic disease in exposed patients is not different from the rate of expected cases. Finally we explore arguments that support and refute a potential biologic relationship between TNFa neutralization and demyelinating disease.
12905465 New radiographic bone erosions in the wrists of patients with rheumatoid arthritis are det 2003 Aug OBJECTIVE: In a 5-year followup study, we investigated the temporal relationship between development of wrist joint erosions as visualized by magnetic resonance imaging (MRI) versus conventional radiography (CR), in patients with rheumatoid arthritis. We also evaluated the risk of erosive progression on CR associated with the presence of MRI erosions. METHODS: In 10 patients with rheumatoid arthritis, MRI and CR of the dominant wrist were performed annually for 5 years. In each image set, each wrist bone (metacarpal bases, carpal bones, radius, and ulna) was assessed for the absence or presence of bone erosions. RESULTS: Nine bones showed radiographic erosions at baseline. Twenty-seven new radiographic erosions developed during the 5-year followup period. Of these 27 new erosions, 21 were detected 1-5 years earlier by MRI than by CR, 3 were simultaneously detected by both methods, 2 were detected 1-2 years later by MRI than by CR, and 1 erosion (radiographically detected at 5-year followup) was not visualized with MRI. MRI detection of new radiographic erosions preceded CR detection by a median of 2 years. In bones with MRI erosions at baseline, the relative risk of radiographic erosions at 5-year followup was 4.5 (95% confidence interval [95% CI] 2.6-7.6), compared with bones without baseline MRI erosions. If bones with baseline radiographic erosions were excluded from the analysis, the relative risk was 4.1 (95% CI 2.2-7.5). CONCLUSION: Most new radiographic bone erosions (78%) were visualized at least 1 year earlier by MRI than by CR. This illustrates that the information on joint destruction provided by CR is considerably delayed compared with that provided by MRI. A significantly increased risk of progression of radiographic erosion in bones with baseline MRI erosions was observed, demonstrating a prognostic value of MRI with respect to long-term radiographic outcome.