Search for: rheumatoid arthritis methotrexate autoimmune disease biomarker gene expression GWAS HLA genes non-HLA genes
ID | PMID | Title | PublicationDate | abstract |
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16205926 | Synovial proinflammatory cytokines and their correlation with matrix metalloproteinase-3 e | 2006 May | The objective of this study has been the well established fact that proinflammatory cytokines and metalloproteinases play a crucial role in the pathogenesis of chronic arthritis as well as the development of pannus, with the eventual erosive changes. Among the proinflammatory cytokines, interleukin-18 (IL-18) has been shown to contribute to the pathogenesis of chronic synovitis by increasing the secretion of interleukin-1beta (IL-1beta) and the tumor necrosis factor-alpha (TNF-alpha) and also stimulating angiogenesis. The aim of this study is to investigate the synovial IL-18, IL-1beta, TNF-alpha and matrix metalloproteinase-3 (MMP-3) levels in patients with Behçet's disease (BD), and compare them with the levels of patients with rheumatoid arthritis (RA) and osteoarthritis (OA). 30 patients with BD, 20 with RA, and 20 with OA were included in the study. The synovial levels of IL-18, IL-1beta, TNF-alpha and MMP-3 were detected using the two-step sandwich ELISA method. The synovial IL-18, TNF-alpha and MMP-3 levels were significantly higher in RA patients than patients with BD (P=0.004, 0.019, 0.025, respectively) and with OA (P=0.004, 0.045, 0.032, respectively). There were no differences, with respect to the cytokine levels, when patients with BD were compared with those with OA. Patients with RA and BD had higher IL-1beta levels than patients with OA (P=0.017, 0.013, respectively). However, no such difference was found for IL-1beta between BD and RA patients. Among patients with RA, positive correlations were found between TNF-alpha and MMP-3 (r=0.683, P=0.001). Our results showed that MMP-3 and proinflammatory cytokines, except IL-1beta, were expressed in relatively small quantities in Behçet's synovitis. Detection of the lower levels of these cytokines and metalloproteinases might explain the non-erosive character of Behçet's arthritis. We suggest that IL-1beta may be involved in the pathogenesis of Behçet's synovitis. | |
17343252 | Heat shock protein 70 membrane expression on fibroblast-like synovial cells derived from s | 2006 Nov | OBJECTIVE: To screen fibroblast-like synovial cells derived from synovial tissue of rheumatoid arthritis (RA) and juvenile idiopathic arthritis (JIA) patients for the membrane expression of the heat shock protein Hsp70. METHODS: We performed flow cytometric (fluorescence-activated cell sorting, or FACS) analysis on fibroblast-like synovial cells of 15 RA patients and three JIA patients to investigate Hsp70 membrane expression. Skin fibroblasts derived from the operation wound (n = 4) and peripheral blood mononuclear cells (PBMC) of seven RA and three JIA patients were also tested. Peripheral blood lymphocytes (PBL) and skin fibroblasts of 10 healthy individuals were used as negative controls. RESULTS: A significantly higher percentage of Hsp70 membrane expression was found on fibroblast-like synovial cells derived from arthritis-affected joints in RA patients (mean 47.7%) when compared with autologous skin fibroblasts (mean 9.5%, p < 0.001) and control skin fibroblasts (mean 5.6%, p < 0.001) or autologous PBL (mean CD45/Hsp70-positive 10.4%, p < 0.001) and control PBL (mean CD45/Hsp70-positive 7.7%, p < 0.001). A high percentage of Hsp70 membrane expression was also observed on fibroblast-like synovial cells derived from three patients with JIA (mean 35.2%) when compared with autologous PBL (mean CD45/Hsp70-positive 10.4%). Synovial cells derived from non-affected joints in a patient with RA who underwent synovectomy for trauma showed low expression of Hsp70 (10.9%). CONCLUSION: Fibroblast-like synovial cells derived from patients with severe course of RA and JIA are strongly positive for membrane-expressed Hsp70. | |
19035506 | Shift from toll-like receptor 2 (TLR-2) toward TLR-4 dependency in the erosive stage of ch | 2008 Dec | OBJECTIVE: Toll-like receptors (TLRs) may activate innate and adaptive immune responses in rheumatoid arthritis (RA) through recognition of microbial as well as endogenous ligands that have repeatedly been found in arthritic joints. The objective of this study was to investigate the involvement of TLR-2 and TLR-4 in the development of chronic destructive streptococcal cell wall (SCW)-induced arthritis, in which interleukin-1 (IL-1)/IL-17-dependent T cell-driven pathologic changes replace the macrophage-driven acute phase. METHODS: Chronic SCW arthritis was induced by 4 repeated intraarticular injections of SCW fragments in wild-type, TLR-2(-/-), and TLR-4(-/-) mice. Clinical, histopathologic, and immunologic parameters of arthritis were evaluated. RESULTS: The TLR-2 dependency of joint swelling during the acute phase was shifted to TLR-4 dependency during the chronic phase. Persistent joint inflammation in the latter phase of the model was significantly suppressed in TLR-4(-/-) mice. In the chronic phase, TLR-4 actively contributed to matrix metalloproteinase (MMP)-mediated cartilage destruction and to osteoclast formation, since the expression of the MMP-specific aggrecan neoepitope VDIPEN and the osteoclast marker cathepsin K was significantly reduced in TLR-4(-/-) mice. Furthermore, TLR-4(-/-) mice expressed less IL-1beta, tumor necrosis factor alpha, IL-6, and IL-23, cytokines that are implicated in IL-17 production. Accordingly, SCW-specific IL-17 production was found to be dependent on TLR-4 activation, since T cells from arthritic TLR-4(-/-) mice produced markedly less IL-17 upon SCW stimulation, whereas interferon-gamma production remained unaffected. CONCLUSION: These data indicate the involvement of TLR-4 in the chronicity and erosive character of arthritis coincident with the antigen-specific IL-17 response. The high position of TLR-4 in the hierarchy of erosive arthritis provides an interesting therapeutic target for RA. | |
17965121 | Synovial tissue response to rituximab: mechanism of action and identification of biomarker | 2008 Jul | OBJECTIVE: To investigate the synovial tissue in patients with rheumatoid arthritis (RA) treated with rituximab and to identify possible predictors of clinical response. METHODS: A total of 24 patients with RA underwent synovial biopsy before, 4 and 16 weeks after initiation of rituximab treatment (without peri-infusional corticosteroids to prevent bias). Immunohistochemical analysis was performed and stained sections were analysed by digital image analysis. Linear regression analysis was used to identify predictors of clinical response. RESULTS: The 28-joint Disease Activity Score (DAS28) was unaltered at 4 weeks, but significantly reduced at 16 and 24 weeks. Serum levels of IgM-rheumatoid factor (RF) decreased significantly at 24 weeks and anti-citrullinated peptide antibody (ACPA) levels at 36 weeks. Peripheral blood B cells were depleted at 4 weeks and started to return at 24 weeks. Synovial B cells were significantly decreased at 4 weeks, but were not completely depleted in all patients; there was a further reduction at 16 weeks in some patients. We found a significant decrease in macrophages at 4 weeks, which was more pronounced at 16 weeks. At that timepoint, T cells were also significantly decreased. The reduction of plasma cells predicted clinical improvement at 24 weeks. CONCLUSIONS: The results support the view that B cells orchestrate local cellular infiltration. The kinetics of the serological as well as the tissue response in clinical responders are consistent with the notion that rituximab exerts its effects in part by an indirect effect on plasma cells associated with autoantibody production, which could help explain the delayed response after rituximab treatment. | |
18593464 | Novel splice variants derived from the receptor tyrosine kinase superfamily are potential | 2008 | INTRODUCTION: Despite the advent of biological therapies for the treatment of rheumatoid arthritis, there is a compelling need to develop alternative therapeutic targets for nonresponders to existing treatments. Soluble receptors occur naturally in vivo, such as the splice variant of the cell surface receptor for vascular endothelial growth factor (VEGF)--a key regulator of angiogenesis in rheumatoid arthritis. Bioinformatics analyses predict that the majority of human genes undergo alternative splicing, generating proteins--many of which may have regulatory functions. The objective of the present study was to identify alternative splice variants (ASV) from cell surface receptor genes, and to determine whether the novel proteins encoded exert therapeutic activity in an in vivo model of arthritis. METHODS: To identify novel splice variants, we performed RT-PCR using an mRNA pool representing major human tissue types and tumors. Novel ASV were identified by alignment of each cloned sequence to its respective genomic sequence in comparison with full-length transcripts. To test whether these ASV have biologic activity, we characterized a subset of them for ligand binding, and for efficacy in an animal model of arthritis. The in vivo study was accomplished using adenoviruses expressing secreted ASV. RESULTS: We cloned 60 novel human ASV from 21 genes, encoding cell surface receptors--many of which are known to be important in the regulation of angiogenesis. The ASV were characterized by exon extension, intron retention and alternative exon utilization. Efficient expression and secretion of selected ASV--corresponding to VEGF receptor type 1, VEGF receptor type 2, VEGF receptor type 3, angiopoietin receptor Tie1, Met (receptor for hepatocyte growth factor), colony-stimulating factor 1 receptor, platelet-derived growth factor receptor beta, fibroblast growth factor receptor 1, Kit, and RAGE--was demonstrated, together with binding to their cognate ligands. Importantly, ASV derived from VEGF receptor type 1 and Tie1, and to a lesser extent from VEGF receptor type 2 and fibroblast growth factor receptor 1, reduced clinical signs of arthritis in vivo. The reduction was paralleled by decreased joint inflammation and destruction. CONCLUSION: The present study shows that unique ASV derived from receptors that play key roles in angiogenesis--namely, VEGF receptor type 1 and, for the first time, Tie1--can markedly reduce arthritis severity. More broadly, our results demonstrate that ASV are a source of novel proteins with therapeutic potential in diseases in which angiogenesis and cellular hyperplasia play a central role, such as rheumatoid arthritis. | |
17407236 | The OMERACT Ultrasound Group: status of current activities and research directions. | 2007 Apr | Ultrasound (US) is a relatively new imaging modality in rheumatology that offers great potential as a diagnostic and management tool. In 2004, an OMERACT Ultrasound Special Interest Group was formed to address the metric qualities of US as a potential outcome measure. A preliminary systematic review highlighted the deficiencies in the literature, particularly with regard to the reliability of interpreting and acquiring images; as a consequence, a number of exercises were proposed to address these issues. This report describes a series of iterative studies that have resulted in improved intra- and inter-reader reliability for detecting and scoring synovitis from both static and real-time images of the hand joints of patients with rheumatoid arthritis. The reliability of acquiring images was also enhanced using standardized positions. Future studies will assess the value of US in clinical trials. | |
17033852 | Ultrasound detects rapid progression of erosive disease in early rheumatoid arthritis: a p | 2007 Feb | OBJECTIVE: To evaluate and compare sequential ultrasound exams (US) with power-Doppler (PD) to radiography for the detection of synovitis and erosions in patients with early RA. METHODS: Radiographs and US with PD of the hands and feet were performed at baseline and 6+/- 2 months afterwards in 21 early RA patients. Their mean (range) age was 42.6 (21-81) years and the female/male ratio was 4:3; mean disease duration was 9 (1-28) months. Joints assessed were bilateral 2nd and 5th MCPs, 5th MTPs and the most swollen PIP in each hand, for a total of eight joints per patient. Radiographs (PA, lateral and pronated oblique) were read for erosions using the method of Sharp/van der Heijde. On US, erosions were defined as cortical defects greater than 2 mm in diameter with an irregular floor. Synovitis was rated as +1 (increase in joint fluid without synovial hyperemia), +2 (mild blood flow), +3 (moderate blood flow), and +4 (severe blood flow). Two blinded trained assessors read all images. RESULTS: US detected 15 erosions in 10 patients at baseline and 31 erosions in 12 patients on follow-up; radiographs could detect only one erosion at baseline and five erosions in three patients on follow-up. PD detected synovitis in all patients at baseline and on follow-up. Of the joints found to have synovitis, 64% were identified as such at baseline and 38% on follow-up. CONCLUSIONS: Sequential US can determine disease progression in patients with early RA. Such data may allow the clinician to treat RA patients earlier in the hope of preventing joint damage. | |
17850683 | Cells of the synovium in rheumatoid arthritis. Dendritic cells. | 2007 | Dendritic cells are the major antigen-presenting and antigen-priming cells of the immune system. We review the antigen-presenting and proinflammatory roles played by dendritic cells in the initiation of rheumatoid arthritis (RA) and atherosclerosis, which complicates RA. Various signals that promote the activation of NF-kappaB and the secretion of TNF and IL-1 drive the maturation of dendritic cells to prime self-specific responses, and drive the perpetuation of synovial inflammation. These signals may include genetic factors, infection, cigarette smoking, immunostimulatory DNA and oxidized low-density lipoprotein, with major involvement of autoantibodies. We propose that the pathogenesis of RA and atherosclerosis is intimately linked, with the vascular disease of RA driven by similar and simultaneous triggers to NF-kappaB. | |
17426140 | The TNF superfamily member LIGHT contributes to survival and activation of synovial fibrob | 2007 Jul | OBJECTIVES: The TNF superfamily member LIGHT has a T-cell co-stimulatory role and has previously been associated with inflammation and autoimmunity. To investigate its role in rheumatoid arthritis (RA), a disease where activated T cells contribute in a prominent way, we have analysed the expression of LIGHT and its receptors in RA and analysed its effects on synovial fibroblasts in vitro. METHODS: The expression of LIGHT was measured in synovial tissues and fluids and the receptors of LIGHT were detected on synovial fibroblasts derived from patients with RA and osteoarthritis (OA). The effects of recombinant LIGHT on the production of proinflammatory cytokines and proteases and on the apoptosis of synovial fibroblasts was assessed. RESULTS: LIGHT mRNA was present in synovial tissues of patients with RA but not with OA. Correspondingly, soluble LIGHT protein could be detected in RA synovial fluid samples at much higher levels than in synovial fluid from patients with OA. Immunohistochemical detection of LIGHT and analysis of synovial fluid cells by flow cytometry revealed CD4 T cells as the major source of LIGHT in the rheumatoid joint. Synovial fibroblasts from RA patients were found to express the LIGHT receptors HVEM and LTbetaR. Recombinant LIGHT induced RA synovial fibroblasts to upregulate MMP-9 mRNA, CD54 and IL-6 in an NF-kappaB-dependent fashion. In vitro, exposure of cultured synovial fibroblasts to LIGHT reduced FAS-mediated apoptosis significantly, without affecting the rate of spontaneous apoptosis. CONCLUSIONS: The results provide evidence for a novel T-cell-dependent activation of synovial fibroblasts by LIGHT in joints of patients with RA, contributing to an inflammatory and destructive phenotype. | |
19110161 | Posterior tibial artery pseudoaneurysm identified subsequent to surgical wound dehiscence. | 2009 Jan | The development of a pseudoaneurysm of the posterior tibial artery is a rare event. In this article, we describe the case of a 63-year-old female with rheumatoid arthritis, who initially presented with a symptomatic subcutaneous nodule localized to the medial aspect of the right ankle. After excision of the subcutaneous nodule, she failed to heal the surgical wound and, eventually, the pseudoaneurysm of the posterior tibial artery was identified. It was not until after the posterior tibial artery was ligated and the pseudoaneurysm excised, that the wound finally healed. LEVEL OF CLINICAL EVIDENCE: 4. | |
17303243 | B cells are important as antigen presenting cells for induction of MHC-restricted arthriti | 2007 Apr | Rheumatoid arthritis and its animal model, collagen-induced arthritis, are known as a T and B cell dependent disease. To analyze the role of B cells in arthritis, we generated B cell deficient (microMT) mice carrying HLA-DQ8 as transgene, Abetao.DQ8.micromt mice. HLA-DQ8 transgenic mice (Abetao.DQ8) are susceptible to collagen induced arthritis, an animal model for inflammatory arthritis. Deletion of IgM gene led to the absence of B cells while T cells were comparable to Abetao.DQ8 mice. Arthritis and autoantibodies was completely abrogated in B cell deficient DQ8 mice. T cell response and proinflammatory cytokine production in response to type II collagen and its derived peptides in vitro was significantly decreased despite an increased number of Mac-1 positive cells in DQ8.micromt mice compared to DQ8 mice suggesting B cells could be important for antigen presentation as well. In vitro substitution of B cells from wild type mice restored the response in DQ8.micromt mice. B cells could also present CII-derived peptides to antigen-specific DQ8-restricted hybridomas reinforcing the role of B cells in presentation of antigens to T cells. The data suggest that B cells can be involved in pathogenesis of arthritis by producing autoantibodies and antigen presentation. | |
18508549 | Recent acquisitions on the genetic basis of autoimmune disease. | 2008 May 1 | In this review we will discuss recent progress from studies on the genetic basis of autoimmune disease and how this has advanced our understanding of the processes behind disease susceptibility and pathogenesis. We review the genetic associations with autoimmune and inflammatory disease discovered in the latest genome-wide association (GWA) scans, and discuss the importance of animal models both for generating candidates and for mechanistic studies. Investigating the natural variants of key immune regulatory molecules can give us an additional level of insight into their function and physiological regulation over gene knockouts. New data showing the association of multiple genes involved in pathogen defense highlights the potential role of infection in autoimmunity, and a more complete understanding of the pathways defective in genetically susceptible individuals will also give us a handle on how environmental and epigenetic factors may be impacting disease. | |
18076664 | Long-term follow-up of patients with tuberculosis as a complication of tumour necrosis fac | 2008 Feb | This study investigated the long-term outcome of patients with tuberculosis (TB) as a complication of tumour necrosis factor (TNF)-alpha blocker therapy. All TB cases (n = 21) complicating TNF-alpha blocker therapy from French university hospitals were collated between January 2000 and September 2002. Outcome was assessed via a postal questionnaire during September 2005. The mortality rate after 4 years was 4.8%, and one patient had relapsed and six (29%) patients had recommenced TNF-alpha antagonist treatment, after appropriate anti-TB therapy, without reactivation. These data support the concept that TNF-alpha antagonists can be restarted in TB patients provided that adequate anti-TB treatment has been completed. | |
19024278 | [Adalimumab (Humira)--efficacy in rheumatoid arthritis treatment with particular reference | 2008 | Tumor-necrosis factor-alpha (TNFalpha) is a pro-inflammatory cytokine demonstrated to play an important role in the pathogenesis of rheumatoid arthritis (RA). Adalimumab is a recombinant human monoclonal antibody to TNFalpha. In the PREMIER study, when administered in combination with methotrexate (MTX), adalimumab demonstrated that 49% patients with early RA achieved remission. Adalimumab was effective in improving radiographic outcomes, too. At week 28, 52 and 104 of follow-up there was significantly less radiographic progression in combination group (adalimumab/MTX) than in each monotherapy group (adalimumab or MTX), with adalimumab showing better result than MTX. In a large open-label study with active RA, during adalimumab treatment 25% of patients experienced clinical remission and nearly half achieved minimal disease activity. Combining results from different clinical trials adalimumab has demonstrated up to seven years of efficacy among long-standing RA patients when used in combination with MTX. The percentage ofpatients achieving clinical remission continued to increase after two or more years of continuous treatment with combination therapy. In Health economic outcome study performed in parallel with PREMIER study there was a big reduction of days lost in the combination group (adalimumab/MTX) in comparison with MTX at year 1 and a difference maintained to year 2. The combination therapy was much more successful in maintaining quality of work than MTX. PROWD study, which was the first one to actually look at job loss as the primary outcome, showed that the combination of adalimumab and methotrexate has the ability to reduce job loss and work time lost when compared to just MTX. Adalimumab is the newest developed anti-TNFalpha, which not only demonstrated significant and sustained reduction in signs and symptoms and inhibition of radiographic progression, but has also improved functional status, quality of life and work productivity in patients with RA, with acceptable safety profile. | |
17392349 | Why are Dutch rheumatologists reluctant to use the COBRA treatment strategy in early rheum | 2007 Jul | BACKGROUND: The Combinatietherapie Bij Reumatoide Artritis (COBRA) trial has proved that combination therapy with prednisolone, methotrexate and sulphasalazine is superior to sulphasalazine monotherapy in suppressing disease activity and radiological progression of early rheumatoid arthritis (RA). In addition, 5 years of follow-up proved that COBRA therapy results in sustained reduction of the rate of radiological progression. Despite this evidence, Dutch rheumatologists seem reluctant to prescribe COBRA therapy. OBJECTIVE: To explore the reasons for the reluctance in Dutch rheumatologists to prescribe COBRA therapy. METHODS: A short structured questionnaire based on social-psychological theories of behaviour was sent to all Dutch rheumatologists (n = 230). RESULTS: The response rate was 50%. COBRA therapy was perceived as both effective and safe, but complex to administer. Furthermore, rheumatologists expressed their concern about the large number of pills that had to be taken, the side effects of high-dose prednisolone and the low dose of methotrexate. Although the average attitude towards the COBRA therapy was slightly positive (above the neutral point), the majority of responding rheumatologists had a negative intention (below the neutral point) to prescribe COBRA therapy in the near future. CONCLUSION: The reluctance of Dutch rheumatologists to prescribe effective COBRA therapy may be due to perceptions of complexity of the treatment schedule and negative patient-related consequences of the therapy. | |
17825098 | Skewed distribution of proinflammatory CD4+CD28null T cells in rheumatoid arthritis. | 2007 | Expanded populations of CD4+ T cells lacking the co-stimulatory molecule CD28 (CD4+CD28null T cells) have been reported in several inflammatory disorders. In rheumatoid arthritis, increased frequencies of CD4+CD28null T cells in peripheral blood have previously been associated with extra-articular manifestations and human cytomegalovirus (HCMV) infection, but their presence in and contribution to joint manifestations is not clear. In the present article we investigated the distribution of CD4+CD28null T cells in the synovial membrane, synovial fluid and peripheral blood of RA patients, and analysed the association with erosive disease and anti-citrullinated protein antibodies. CD4+CD28null T cells were infrequent in the synovial membrane and synovial fluid, despite significant frequencies in the circulation. Strikingly, the dominant TCR-Vbeta subsets of CD4+CD28null T cells in peripheral blood were often absent in synovial fluid. CD4+CD28null T cells in blood and synovial fluid showed specificity for HCMV antigens, and their presence was clearly associated with HCMV seropositivity but not with anti-citrullinated protein antibodies in the serum or synovial fluid, nor with erosive disease. Together these data imply a primary role for CD4+CD28null T cells in manifestations elsewhere than in the joints of patients with HCMV-seropositive rheumatoid arthritis. | |
16687338 | Long term results of arthrodesis of the wrist: a 6-15 year follow up of 35 patients. | 2006 | A total of 40 wrists in 35 patients were investigated 10.5 (range 6-15) years after arthrodesis. The most common diagnosis was rheumatoid disease. There were 21 Mannerfelt, and 21 plate, arthrodeses. The patients were assessed clinically and up-to-date radiographs obtained. Two Mannerfelt arthrodeses had failed to fuse. Pain during the last week before review and total satisfaction with the operation were excellent in 28 and 30 wrists, respectively. The mean score on the "Disability of arm, shoulder and hand" (DASH) questionnaire was 38 (range 2-75). Plate arthrodeses gave better results than Mannerfelt arthrodeses for all variables studied. Wrists plated in dorsal extension gave the best scores for function and strength. We conclude that either method gives good long term results. Although few of the individual differences were statistically significant, we think that fusion with plates, and in particular plates with dorsal extension, is preferable. | |
18336873 | Bone marrow edema in the cervical spine of symptomatic rheumatoid arthritis patients. | 2009 Feb | OBJECTIVE: To investigate the frequency and clinical significance of bone marrow edema (BME) in a series of patients with rheumatoid arthritis (RA) and symptomatic involvement of the cervical spine. METHODS: We studied 19 consecutive RA patients with cervical spine magnetic resonance imaging (MRI) according to a specifically designed protocol that included short inversion time inversion recovery sequences. All cases had neck pain unresponsive to conventional treatment, neurological symptoms, or signs suggestive of cervical myelopathy, or cervical pain with evidence of atlantoaxial subluxation on radiographs. RESULTS: The mean age of the 19 patients (15 women and 4 men) at time of the study was 59 +/- 12 years (range, 23-82) and the median disease duration was 14 +/- 7.4 years (range, 4-30). BME was observed in 74% (14/19) of the patients: at the atlantoaxial level alone in 16% of the patients; subaxially alone in 16%; and at both levels in 42% of the patients. At the atlantoaxial level, BME was usually observed involving the odontoid process, whereas subaxially BME was limited to the vertebral plates and the interapophyseal joints. Patients with BME had higher erythrocyte sedimentation rate (ESR) values at the time of MRI examination (P = 0.014) and more severe atlantoaxial joint MRI synovitis scores (P = 0.05) compared with the remaining patients; the frequency of odontoid erosions was also greater in this group, but the difference did not reach statistical significance. Altogether, these data suggest a more severe inflammatory response in these patients. In this group a significant correlation was found between BME scores at atlantoaxial level and (1) ESR values (r = 0.854; P = 0.001) and (2) atlantoaxial joint MRI synovitis scores (r = 0.691; P = 0.001). CONCLUSION: BME is frequently observed in patients with established RA and symptomatic cervical spine involvement. Both atlantoaxial and subaxial levels are equally affected. The presence of BME seems related to the intensity of the inflammatory response and to the severity of the atlantoaxial joint synovitis. | |
18322989 | Comparison of internal and external responsiveness of the generic Medical Outcome Study Sh | 2008 Apr | OBJECTIVE: To examine the comparative internal and external responsiveness of the generic Medical Outcome Study Short Form-36 Health Survey (SF-36) and disease-specific measures in patients with rheumatoid arthritis (RA). METHODS: Data were collected from 280 RA patients starting anti-tumor necrosis factor treatment. A total of 168 patients completed a questionnaire including the SF-36, the Arthritis Impact Measurement Scales 2 (AIMS2), the Health Assessment Questionnaire (HAQ), a visual analog scale for general health (VAS-GH), and an 11-point numerical rating scale for pain (NRS pain) at baseline and after 12 months. Internal responsiveness was evaluated with paired samples t-tests and standardized response means (SRM). External responsiveness was investigated with receiver-operating characteristic statistics and Spearman rank-order correlation coefficients. A health transition item was used as the external indicator of change. RESULTS: No significant differences in internal and external responsiveness were found between the SF-36 and disease-specific measures within the domains physical function, pain, and psychological function. In the domain social function, the SF-36 was more responsive than the AIMS2. In the domain general health, the SF-36 was less responsive (only internal) than the AIMS2 and VAS-GH. CONCLUSION: Our study showed comparable internal and external responsiveness of the SF-36 compared with disease-specific measures (AIMS2, HAQ, NRS pain) in all health domains, except social function and general health domains. The assumption that disease-specific measures are more responsive to detect intervention-related changes over time is not confirmed by our data. | |
17216012 | [Does magnetic resonance represent the future in the follow-up of arthritis?]. | 2006 Oct | Several studies suggest that MRI is between 2 and 10 times superior to conventional radiology in the visualization of erosions. This higher sensibility is dependent on the specific joint assessed, the precocity of the disease, and the timing of follow-up. In addition, MRI can depict bone oedema, which is an early and reversible bone lesion, and evaluate the degree of inflammation of the synovial membrane. A single examination could therefore evaluate disease activity and damage. The sensitivity to change of articular MRI is good, as demonstrated by a number of follow-up studies. In view of these advantages, it may be surprising that MRI has not yet become the gold standard of imaging of the arthritic joint. The three main reasons are low availability of high field machines, examination's costs, and lack of standardization of the technique. Low field extremity-dedicated MRI machines are probably the answer to the first two concerns. They have been shown to obtain reliable results for the clinician, and to be relatively cheap and patient-friendly, allowing repeated follow-up examinations. As far as standardization is concerned, there are many studies addressing the problem, with OMERACT as the driving force. MRI is likely to represent the future of the follow up of arthritis for the evaluation of its pace of progression and the effect of treatment. The advent of new and potent biologic therapies has incremented the need for more sensible imaging methods and will probably drive their diffusion in clinical practice. |