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ID PMID Title PublicationDate abstract
12138804 [Nimesil effectiveness in rheumatoid arthritis]. 2002 Clinical efficiency and safety of nimesil were studied in the multicenter open clinical trial of 52 patients with verified rheumatoid arthritis. Nimesil was given for 12 weeks in a daily dose 200-400 mg in addition to basic therapy. Clinical and laboratory parameters were assessed after 4 and 8 weeks of the treatment and after its end. The treatment produced a significant positive response of the articular syndrome. Marked improvement was registered in 11 (23.4%) patients, improvement--in 33 (79.2%) patients. Side effects were reversible and occurred in 8 (15.3%) patients. In 5 patients the drug was withdrawn. The conclusion is made on high efficiency and good tolerance of nimesil in rheumatoid arthritis patients.
12407423 Inhibition of cartilage destruction by double gene transfer of IL-1Ra and IL-10 involves t 2002 Nov The objective of the study was to determine the effects and the molecular background of interleukin-1 receptor antagonist (IL-1Ra) and vIL-10 double gene transfer into human synovial fibroblasts from patients with rheumatoid arthritis (RA) using the SCID mouse model for cartilage erosion in RA. RA synovial fibroblasts were transduced with retro- or adenoviruses encoding IL-1Ra and/or viral IL-10 (vIL-10). SCID mice were engrafted subcutaneously with IL-1Ra and vIL-10 transduced human rheumatoid synovial fibroblasts and normal cartilage. In parallel, gene expression analysis before and after gene transfer using RNA arbitrarily primed PCR in combination with cDNA array was performed. vIL-10 and IL-1Ra double gene transfer resulted in inhibition of cartilage invasion and degradation by RA synovial fibroblasts when compared with control transduced and non-transduced implants. Expression of key genes that were altered after double gene transfer were related to the activin pathway. The results demonstrate not only that virus-based gene transfer using a combination of two joint-protective genes is a feasible approach to inhibit cartilage degradation by activated RA synovial fibroblasts, but also that the underlying molecular effects include modulation of the activin pathway.
12114276 Delayed neutrophil apoptosis induced by synovial fluid in rheumatoid arthritis: role of cy 2002 Jun The fate of neutrophils at sites of inflammation, where these cells are likely exposed to both anti- and proapoptotic influences, needs to be clarified. To investigate this issue, we studied the survival of neutrophils in the presence of articular fluids from RA joints before and after immune complex activation. Eight of eleven samples of RA synovial fluid studied were found to inhibit spontaneous and immune complex-stimulated neutrophil apoptosis. No relationships were found between GM-CSF and TNF-alpha concentrations measured on each sample of synovial fluid studied and the levels of neutrophil apoptosis detectable in the presence of the same synovial fluid. Furthermore, no activity on neutrophil survival was observed at either physiologic or pharmacologic concentrations of estradiol. On the contrary, the synovial fluid anti-apoptotic activity correlates (r(2) = 0.8818, p < 0.0001) with the adenosine detected at concentrations in each sample ranging from 18.7 to 52.4 microM. Finally, synovial fluids were incapable of interfering with neutrophil activation evaluated as superoxide anion production. Our results suggest that the microenvironment of rheumatoid synovial fluid is a proinflammatory milieu responsible for the in loco persistence of activated and long-surviving neutrophils.
12676609 Ecologic analysis of some immune-related disorders, including type 1 diabetes, in Australi 2003 Apr The apparent immune-suppressive effect of ultraviolet radiation (UVR) has suggested that this environmental exposure may influence the development of immune-related disorders. Self-reported prevalence rates of type 1 diabetes mellitus, rheumatoid arthritis (RA), eczema/dermatitis, and asthma, from the 1995 Australian National Health Survey, were therefore examined by latitude and ambient level of UVR. A positive association of type 1 diabetes mellitus prevalence was found with both increasing southern latitude of residence (r = 0.77; p = 0.026) and decreasing regional annual ambient UVR (r= -0.80; p = 0.018); a 3-fold increase in prevalence from the northernmost region to the southernmost region was evident. In contrast, asthma correlated negatively with latitude (r = -0.72; p = 0.046), although the change in asthma prevalence from the north to the south of Australia was only 0.7-fold. For both RA and eczema/dermatitis, there were no statistically significant associations between latitude/UVR and disease prevalence. These ecologic data provide some support for a previously proposed beneficial effect of UVR on T-helper 1-mediated autoimmune disorders such as type 1 diabetes. The inverse association of type 1 diabetes prevalence with UVR is consistent with that previously reported for another autoimmune disease, multiple sclerosis, in Australia, and also with type 1 diabetes latitudinal gradients in the Northern Hemisphere. The finding also accords with photoimmunologic evidence of UVR-induced immunosuppression and may suggest a beneficial effect of UVR in reducing the incidence of such autoimmune conditions. In light of this study, analytic epidemiologic studies investigating risk of immune disorders in relation to personal UVR exposure in humans are required.
12508773 Interleukin-10 expression: is there a neglected contribution of CD8+ T cells in rheumatoid 2002 Nov OBJECTIVE: To search for RA specific processes among T cell accumulation, T cell activation, or cytokine expression in CD4+ and CD8+ synovial fluid (SF) T cells. METHODS: Flow cytometry of CD4+, CD8+, CD45RA+, CD45RO+, CD69 double or triple stained peripheral blood (PB) and SF T cells. IL-2, IL-10, and IFN-gamma expression was determined in PMA + ionomycin stimulated T cells on the single cell level. Concentrations of secreted IL-2, IL-4, IL-10, and IFN-gamma were quantified in the sera and synovial fluids by enzyme linked immunosorbent assay (ELISA). RESULTS: A preferential recruitment of CD45RO+ memory T cells was found for CD4+ helper T cells, and in similar also for CD8+ suppressor T cells. An elevated CD69 expression was detected in memory, but also in CD45RA+ naive CD4+ and CD8+ SF T cells, whilst IL-2 expression was only demonstrable in a minor proportion of T cells populations. Preferential recruitment of memory T cells, but incomplete activation of naive and memory, CD4+ and CD8+ T cells were in similar found in RA and control patients. In RA but not in the control patients, a relevant proportion of CD4+ and CD8+ PB and SF T cells expressed IL-10 and IFN-gamma. High concentrations of IL-10, that were correlated with the amounts of secreted TNF-alpha, were only detected in RA joints. CONCLUSION: Memory and naive T cell state of CD4+ and CD8+ T cell accumulates in the joints, and early T cell activation occur in similar patterns in RA and control patients. High IL-10 SF concentrations in contrast, and elevated percentages of IFN-gamma and IL-10 expressing CD4+ and CD8+ T cells in the PB and SF were characteristic for RA. Here, CD8+ T cells may contribute to high IL-10 concentrations in RA joints.
12384916 Hypoxia-induced production of stromal cell-derived factor 1 (CXCL12) and vascular endothel 2002 Oct OBJECTIVE: Stromal cell-derived factor 1 (SDF-1; or, CXCL12) is a potent chemotactic and angiogenic factor that has been proposed to play a role in the recruitment of lymphocytes into rheumatoid arthritis (RA) synovium. We tested the hypothesis that synovial SDF-1 expression is regulated by cytokine and hypoxic stimulation, the latter being mediated by hypoxia-inducible factor 1alpha (HIF-1alpha). These factors regulate the expression of vascular endothelial growth factor (VEGF), itself an important angiogenic mediator. METHODS: RA and osteoarthritic synovial fibroblasts and whole tissue explants were cultured under normoxic or hypoxic (1% O(2)) conditions for up to 72 hours in the presence or absence of interleukin-1beta (IL-1beta), tumor necrosis factor (TNF), or transforming growth factor beta (TGFbeta). Expression of HIF-1alpha, VEGF, and SDF-1 was detected in synovial tissue and cells by immunohistochemistry and Western blotting. VEGF and SDF-1 expression by cultured synovial fibroblasts was evaluated by reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay. RESULTS: Immunohistochemistry revealed the presence of HIF-1alpha, VEGF, and SDF-1 in RA synovium. Patchy expression of HIF-1alpha was detected primarily in the synovial lining and sublining areas; expression in synovial fibroblasts and in the lining cells of whole synovial tissue explants was markedly augmented by hypoxic culture conditions. Hypoxia enhanced the expression of VEGF and SDF-1 messenger RNA in synovial fibroblasts. The production of VEGF and SDF-1 protein by synovial fibroblasts was augmented by 50% and 132%, respectively, after 24 hours of hypoxia. VEGF production was potently induced by TGFbeta, and to a lesser extent by IL-1beta and TNF, and was further augmented by hypoxia. In contrast, none of the tested cytokines induced SDF-1 production. CONCLUSION: As with VEGF, SDF-1 expression is induced by hypoxia; however, cytokines induce VEGF but not SDF-1. Hypoxic conditions in RA synovium, which are likely to be transient and episodic, may contribute to the persistence of synovitis by inducing VEGF and SDF-1.
12874640 [Kidney involvement in rheumatoid arthritis]. 2003 Rheumatoid Arthritis (RA) is a widespread disease and its renal involvement, relatively common, is clinically significant because worsens course and mortality of the primary disease. There is still no agreement on the prevalence of renal disorders in RA: data analysis originates from different sources, as death certificates, autopsies, clinical and laboratory findings and kidney biopsies, each with its limitations. Histoimmunological studies on bioptical specimens of patients with RA and kidney damage, led to clarify prevalent pathologies. In order of frequency: glomerulonephritis and amyloidosis (60-65% and 20-30% respectively), followed by acute or chronic interstitial nephritis. Kidney injury during RA includes secondary renal amyloidosis, nephrotoxic effects of antirheumatic drugs and nephropathies as extra-articular manifestations (rheumatoid nephropathy). Amyloidosis affects survival, increases morbidity and is the main cause of end stage renal disease in patients with RA and nephropathy. Strong association between RA activity and amyloidosis needs the use of immunosuppressive and combined therapies, to prevent this complication and reduce risk of dialysis. Long-lasting and combined RA pharmacotherapy involves various renal side effects. In this review we describe NSAIDs and DMARDs (Disease-Modifying Antirheumatic Drugs) nephrotoxicity, particularly by gold compounds, D-penicillamine, cyclosporine A and methotrexate. Rare cases of IgA glomerulonephritis during immunomodulating therapy with leflunomide and TNF blocking receptor (etanercept) are reported; real clinical significance of this drug-related nephropathy will be established by development of RA treatment. In RA nephropathies, mesangial glomerulonephritis is the most frequent histological lesion (35-60 % out of biopsies from patients with urinary abnormalities and/or kidney impairment), followed by minimal change glomerulopathy (3-14%) and p-ANCA positive necrotizing crescentic glomerulonephritis.
15172043 Treatment of rheumatoid arthritis with etanercept. 2004 May Etanercept is effective in the treatment of rheumatoid arthritis (RA)when used as monotherapy and in combination with methotrexate(MTX). Radiographic progression of disease was slowed significantly when the drug was used for a 24-month period and was statistically significantly better than MTX. In addition to its use in RA,etanercept is approved by the U.S. Food and Drug Administration for other rheumatologic conditions, including psoriatic arthritis,ankylosing spondylitis, and juvenile chronic arthritis.
12180717 Antirheumatic effects of humanized anti-Fas monoclonal antibody in human rheumatoid arthri 2002 Aug OBJECTIVE: Anti-Fas monoclonal antibodies (Mab) are considered to be a potential therapeutic agent for rheumatoid arthritis (RA). However, Fas mediated liver and chondrocyte damage is a serious problem in its clinical application. m-HFE7A, a novel anti-Fas Mab, selectively induces apoptosis in inflammatory cells. We succeeded in humanizing m-HFE7A to obtain h-HFE7A. We investigated the therapeutic effects of h-HFE7A Mab in RA. METHODS: We investigated the apoptosis-inducing activities of h-HFE7A on human Fas ligand transfected cells and cultured human activated lymphocytes (human peripheral blood mononuclear cells and isolated human RA synovial lymphocytes), synoviocytes, and chondrocytes. We then examined the effects of h-HFE7A Mab in vivo using SCID-HuRAg mice implanted with human RA tissue. RESULTS: Administration of h-HFE7A Mab alone did not induce apoptosis in cultured human Fas ligand transfected cells and activated lymphocytes. However, apoptosis-inducing activities were noted by this Mab crosslinking with a secondary antibody or Fcgamma receptor positive cells. In contrast, no apoptosis induction by h-HFE7A was observed on cultured synoviocytes and chondrocytes with or without crosslinking. Thus the crosslinking with Fcgamma receptor positive cells is essential for the efficacy of this Mab in vivo. In the implanted tissue of the SCID-HuRAg mice, the number of inflammatory cells was significantly decreased in the h-HFE7A Mab treated group compared to the IgG treated control group. Moreover, there were only negligible effects in synoviocytes and chondrocytes with the h-HFE7A Mab. CONCLUSION: Administration of this novel humanized anti-Fas Mab may provide a new treatment for RA by inducing Fas mediated apoptosis in inflammatory cells.
15004722 The production of CXCR3-agonistic chemokines by synovial fibroblasts from patients with rh 2005 Jun The inflamed synovial tissue of rheumatoid arthritis (RA) is characterized by an infiltration with Th1 cells that predominantly express the chemokine receptors CXCR3 and CCR5. In this study, we investigated the production of the CXCR3-agonistic chemokines CXCL9, CXCL10, and CXCL11 by synovial tissue cells and synovial fibroblast-cell lines (fourth or fifth passage) from RA patients. Concentrations of all CXCR3 ligands in synovial fluids were markedly higher in RA patients than in osteoarthritis (OA) patients. Synovial tissue cells from RA patients more strongly expressed mRNAs for CXCR3 ligands and spontaneously secreted larger amounts of these chemokine proteins than the cells from OA patients. The mRNA expression of all CXCR3 ligands was induced in synovial fibroblasts from RA patients after stimulation with interferon gamma (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), or interleukin-1 beta (IL-1beta). However, synovial fibroblasts significantly secreted CXCL9 and CXCL10 proteins, but not CXCL11 protein, after IFN-gamma stimulation and secreted only CXCL10 protein after TNF-alpha or IL-1beta stimulation. When stimulated with a combination of IFN-gamma and TNF-alpha, these cells were able to secrete large amounts of all three chemokines. These results indicate that synovial fibroblasts may be involved in perpetuating the Th1 immune response by producing the Th1-associated CXCR3 ligands, and the synergistic effect of IFN-gamma and TNF-alpha may be important for their chemokine production in RA joints.
15103675 Suppressive effects of Stephania tetrandra on the neutrophil function in patients with rhe 2004 Mar Crude preparations of Stephania tetrandra (ST), a traditional herbal medicine, have been used safely for arthritis and silicosis in China. The concentration of granulocyte elastase - alpha 1 protease inhibitor complex in plasma is enhanced in inflammatory processes, e.g. in septicaemia and rheumatoid arthritis (RA), being an expression of granulocyte activation during inflammatory response. It has previously been reported that ST showed beneficial and immunomodulatory effects in the treatment of relatively mild RA. After the administration of ST for 12 weeks, the proportion of granulocytes and the granulocyte count in peripheral blood decreased significantly. The lipid peroxide and human granulocyte elastase levels of stored plasma declined significantly. Furthermore, both the leukocyte/elastase ratio and granulocyte/elastase ratio increased significantly. The findings of this study suggest that the suppressive effect of ST administration on excessive granulocyte activation resulted in the improvement of inflammation with rheumatoid arthritis.
11840439 Expression of extracellular matrix metalloproteinase inducer and enhancement of the produc 2002 Feb OBJECTIVE: To investigate the expression of extracellular matrix metalloproteinase inducer (EMMPRIN) at sites of joint destruction in rheumatoid arthritis (RA) and to correlate it with the production of matrix metalloproteinases (MMPs). METHODS: Reverse transcription-polymerase chain reaction was performed to study the existence of EMMPRIN in synovial tissue derived from RA and osteoarthritis (OA) patients. In situ hybridization with a human complementary DNA specific for EMMPRIN and immunohistochemistry were performed to characterize the EMMPRIN-expressing cells at sites of joint destruction, including bone. Northern blot analysis was performed to detect the level of expression of EMMPRIN messenger RNA (mRNA) in synovial tissue. The production of MMP-1 and MMP-3 by synovial tissue from RA patients was examined by enzyme-linked immunosorbent assay. RESULTS: Expression of EMMPRIN mRNA was detected in synovium from 9 of 11 patients with RA and 1 of 5 patients with OA. The presence of mRNA encoding EMMPRIN was recognized in the invasive synovium at sites of joint destruction in RA but not OA. Fibroblast-like synovial cells and granulocytes were demonstrated to express EMMPRIN mRNA. MMP-1 and MMP-3 production by synovial tissue was correlated with levels of expression of EMMPRIN mRNA, as detected by Northern blotting. CONCLUSION: The expression of EMMPRIN stimulates the production of MMP-1 and MMP-3 in the synovial tissue of affected joints in RA. The results of this study suggest that EMMPRIN may be one of the important factors in progressive joint destruction in RA.
15133778 Drug switching patterns among patients with rheumatoid arthritis and osteoarthritis using 2004 May PURPOSE: To compare RA and OA patients' time-to-switch after newly initiating treatment with three most commonly used non-specific (NS)-NSAIDs and two COX-2 inhibitors, celecoxib and rofecoxib. METHODS: Managed care enrollees newly prescribed celecoxib, rofecoxib, ibuprofen, naproxen or diclofenac were identified. Time to switch to a different NS-NSAID or COX-2 specific inhibitor was determined using time-to-event analysis and Cox proportional hazards models were used to estimate the odds ratio (OR) after controlling for potential confounders. RESULTS: The time to 25% of the cohort switching was longer for rofecoxib and celecoxib (159 and 205 days respectively) compared to the three NS-NSAIDs (49-78 days). Patients were at the highest risk of switching within the first 100 days of therapy. After adjusting for potential confounding factors, the OR for switching to another NS-NSAID or COX-2 specific inhibitor ranged from 1.74 to 2.35 for the three NS-NSAIDs compared to celecoxib (all comparisons, p < 0.01). Similar findings were obtained when comparing rofecoxib to each of the three NS-NSAIDS (all comparisons, p < 0.01). When COX-2 inhibitors combined were compared to NS-NSAIDS combined, the OR for switching was 1.53 (95% confidence interval = 1.42-1.65; p < 0.01) after adjusting for potential confounders. CONCLUSIONS: Patients on the COX-2 specific inhibitors (celecoxib and rofecoxib) were significantly less likely to switch their therapy than patients on NS-NSAIDS (ibuprofen, naproxen and diclofenac). These results suggest that COX-2 specific inhibitors may be a more effective treatment option when compared with NS-NSAIDs in usual clinical practice.
12728431 Observations on retrieved glenoid components. 2003 Apr To obtain more information on the pattern of damage of prosthetic glenoid components, we analyzed 7 retrieved glenoid components. The consecutive series included 2 standard polyethylene components and 5 highly crystalline polyethylene glenoids (Hylamer; DePuy Dupont Orthopaedics, Warsaw, IN) retrieved 3 to 12 years after implantation. At revision, 4 of 5 Hylamer components were fractured. Common wear patterns were i) deformation and crumbling of the rim, particularly at the inferior hemicircumference, probably caused by direct contact of the humerus with the prosthetic component; ii) roughening (abrasion and scratching) of the adjacent articulating surface; and iii) concentric and congruous wear centered posteriorly. Available glenoid components may cover an excessive sector of the head. This can result in mechanical restriction of glenohumeral motion and abutment of the humerus against the glenoid rim. Abutment may cause major shear forces and therefore cause glenoid loosening. The value of articular surface mismatch is questionable because retrieved glenoids were worn to a conforming joint.
15180890 Roles of B cells in rheumatoid arthritis. 2003 B lymphocytes play several critical roles in the pathogenesis of rheumatoid arthritis. They are the source of the rheumatoid factors and anticitrullinated protein antibodies, which contribute to immune complex formation and complement activation in the joints. B cells are also very efficient antigen-presenting cells, and can contribute to T cell activation through expression of costimulatory molecules. B cells both respond to and produce the chemokines and cytokines that promote leukocyte infiltration into the joints, formation of ectopic lymphoid structures, angiogenesis, and synovial hyperplasia. The success of B cell depletion therapy in rheumatoid arthritis may depend on disruption of all these diverse functions.
15308516 Diagnostic and clinical value of anti-cyclic citrullinated peptide antibodies compared wit 2004 Sep OBJECTIVE: To assess the additional diagnostic and clinical value of the second test generation of anti-cyclic citrullinated peptide antibodies (CCP2) compared with rheumatoid factor isotypes (IgG-RF, IgA-RF, IgM-RF) in patients with rheumatoid arthritis. METHODS: This was a prospective study on 715 patients: rheumatoid arthritis (n = 295), degenerative or other inflammatory joint disease (n = 163), connective tissue disease or vasculitis (n = 103), and healthy controls (n = 154). Sera from each subject were tested for CCP2 and RF isotypes by enzyme linked immunosorbent assay (ELISA). Agreement with clinical indices such as disease activity, joint destruction, disease duration, and other laboratory tests was assessed. Sensitivity and specificity of the tests were evaluated taking the clinical diagnosis as the gold standard. RESULTS: Highest sensitivity was found for IgM-RF (66.4%) and CCP (64.4%). Highest specificity was achieved by CCP (97.1%) and IgG-RF (91.0%). In rheumatoid patients with high disease activity or severe joint damage, CCP was more often present (81.4% and 83.6%) than all RF isotypes. Of special diagnostic value was the detection of positive CCP in 34.5% of all patients with rheumatoid arthritis when all measured RF isotypes (IgG-RF, IgA-RF, and IgM-RF) were negative. CONCLUSIONS: As a screening method for rheumatoid arthritis the IgM-RF and the CCP assays are superior to other RF isotypes. Positivity in the highly specific CCP ELISA supports the diagnosis of rheumatoid arthritis. CCP proved to be a powerful diagnostic tool, especially in ambiguous cases or RF negative patients with rheumatoid arthritis.
15061573 B-cell biology. 2004 Feb In recent years, our understanding of B-cell biology and the roles of B cells in normal immune responses and autoimmunity has increased dramatically. We no longer think of B cells simply as antibody factories. It is clear that these diverse and exquisitely regulated cells may contribute in a multitude of ways to immune responses. Animal models, clinical trials of biologic agents, and the ever expanding field of molecular biology have made great contributions to our current knowledge. With this improved understanding, we are afforded the opportunity to consider numerous potential therapeutic targets for treating autoimmune disease. As this growing science evolves, we can expect to see the advent of new therapies and new hope for patients who are afflicted with these disorders.
15188349 Lymphoma in rheumatoid arthritis: the effect of methotrexate and anti-tumor necrosis facto 2004 Jun OBJECTIVE: The risk of lymphoma is increased in patients with rheumatoid arthritis (RA), and spontaneous reporting suggests that methotrexate (MTX) and anti-tumor necrosis factor (anti-TNF) therapy might be associated independently with an increased risk of lymphoma. However, data from clinical trials and clinical practice do not provide sufficient evidence concerning these issues because of small sample sizes and selected study populations. The objective of this study was to determine the rate of and standardized incidence ratio (SIR) for lymphoma in patients with RA and in RA patient subsets by treatment group. Additionally, we sought to determine predictors of lymphoma in RA. METHODS: We prospectively studied 18,572 patients with RA who were enrolled in the National Data Bank for Rheumatic Diseases (NDB). Patients were surveyed biannually, and potential lymphoma cases received detailed followup. The SEER (Survey, Epidemiology, and End Results) cancer data resource was used to derive the expected number of cases of lymphoma in a cohort that was comparable in age and sex with the RA cohort. RESULTS: The overall SIR for lymphoma was 1.9 (95% confidence interval [95% CI] 1.3-2.7). The SIR for biologic use was 2.9 (95% CI 1.7-4.9) and for the use of infliximab (with or without etanercept) was 2.6 (95% CI 1.4-4.5). For etanercept, with or without infliximab, the SIR was 3.8 (95% CI 1.9-7.5). The SIR for MTX was 1.7 (95% CI 0.9-3.2), and was 1.0 (95% CI 0.4-2.5) for those not receiving MTX or biologics. Lymphoma was associated with increasing age, male sex, and education. CONCLUSION: Lymphomas are increased in RA. Although the SIR is greatest for anti-TNF therapies, differences between therapies are slight, and confidence intervals for treatment groups overlap. The increased lymphoma rates observed with anti-TNF therapy may reflect channeling bias, whereby patients with the highest risk of lymphoma preferentially receive anti-TNF therapy. Current data are insufficient to establish a causal relationship between RA treatments and the development of lymphoma.
12483720 The geometric architecture of the subtalar and midtarsal joints in rheumatoid arthritis ba 2002 Dec OBJECTIVE: To compare in vivo the 3-dimensional (3-D) geometric architecture of the subtalar and midtarsal joints in normal and rheumatoid arthritic (RA) feet, using magnetic resonance imaging (MRI) analysis. METHODS: MRI was performed on 23 patients with RA, all of whom had disease activity in the subtalar and/or midtarsal joints. Image processing techniques were used to create 3-D reconstructions of the calcaneus (C), cuboid (c), navicular (N), and talus (T) bones. Twenty-four standard architectural parameters were measured from the reconstructions and were compared with data from 10 normal subjects. These parameters defined both 3-D distance and angular relationships among the 4 bones studied. Pattern classification techniques were used to establish a geometric architecture foot profile for the RA patients. The degree of individual patient fit to the new RA foot profile and to profiles for normal, pes planus, and pes cavus foot types was derived. Logistic regression was used to examine the relationship of foot architecture to inflammatory disease characteristics and physical examination variables. RESULTS: Subtalar or midtarsal pain was reported by all 23 patients, and 22 of the 23 patients presented with >/=1 clinical feature of pes planovalgus deformity. In 21 patients, ultrasonography revealed synovitis at >/=1 tarsal joint or surrounding tendon. In the RA group, the normalized distances between the geometric centroids were significantly closer for bone pairs Cc and cT and significantly distracted for bone pair CN compared with the distances in normal subjects. In RA patients (versus normal subjects), the angles subtended at the bone centroids were significantly decreased in 3 bone groups (CNc, TCN, and TNc) and significantly increased in 3 bone groups (CcN, CcT, NTc). The angles formed between the major principal axes of bone pairs CT and cT were significantly increased in RA patients compared with those in normal subjects. Pattern classification defined 11 RA feet as having normal structure and 12 as having abnormal structure. However, the abnormal feet did not fit consistently with structures defined for RA, pes planus, or pes cavus foot types. Logistic regression demonstrated that subtalar joint synovitis was the only predictive factor for abnormal subtalar and midtarsal architecture (odds ratio 19.2, 95% confidence interval 1.77-200.0). CONCLUSION: This unique 3-D MRI-based technique successfully quantified the effects of RA on the geometric architecture of the foot and the patient-specific nature of these changes. This technique can be used to provide logical therapy for correction.
12626792 Psychometric properties of a Dutch short form of the Arthritis Impact Measurement Scales 2 2003 Mar OBJECTIVE: To evaluate the reliability and validity of a Dutch version of the Arthritis Impact Measurement Scales 2 short form (AIMS2-SF) and examine the agreement between the AIMS2 and AIMS2-SF in rheumatoid arthritis (RA) patients. METHODS: Data were collected from 587 RA patients from three studies. Patients completed the Dutch-AIMS2, Modified Health Assessment Questionnaire (M-HAQ), and Visual Analogue Scale for pain (VAS-pain), and clinical data were collected to calculate the Disease Activity Score 28 (DAS28). Short-form component scores were calculated from the AIMS2 long-form data. In addition, a Modified Symptom component score was calculated by replacing item 42 with item 38 as was suggested by Haavardsholm et al. [7] for the Norwegian version. RESULTS: The internal consistency of the Physical, Symptom and Affect components was good (Cronbach's alpha= 0.75-0.87), moderate for the Role component (alpha=0.62) but rather low for the Social Interaction (0.51) component. Replacing item 33 with item 31 of the long-form AIMS2 increased internal consistency for the Social Interaction component to 0.63. Test-retest reliability of the AIMS2-SF components was high (intraclass correlation coefficients >0.70). Mean scores of the AIMS2-SF were generally close to those from the AIMS2, but the limits of agreement were rather wide. Both the Modified Symptom and Modified Social Interaction components showed better agreement than the original short-form components. Plots of differences between AIMS2 and AIMS2-SF against the mean of the two scores for the five components showed that the differences varied over the range of the measurements. Factor analysis confirmed the three-factor structure, with a physical, psychological and social dimension that has been found for the Dutch-AIMS2 long form. Correlations of the AIMS2-SF components with M-HAQ total score, functional class, VAS-pain and DAS28 were very similar to the correlations for the original AIMS2. CONCLUSION: The Dutch-AIMS2-SF, with Modified Symptom and Social Interaction components has good psychometric properties, similar to those of the Dutch-AIMS2 long form.