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ID PMID Title PublicationDate abstract
18322991 Clinical outcome and imaging changes after intraarticular (IA) application of etanercept o 2008 Apr OBJECTIVE: To assess the magnetic resonance imaging (MRI) and ultrasound (US) changes in the wrist of patients with rheumatoid arthritis (RA) 4 weeks after an US guided intraarticular (IA) injection. METHODS: Contrast enhanced MRI and US-Doppler were performed at baseline and 4 weeks after IA injection of either 40 mg methylprednisolone (n = 12) or 25 mg etanercept (n = 13) in 25 patients with RA taking disease modifying antirheumatic drugs with a therapy-resistant wrist joint. All injections were US guided. RESULTS: There was an improvement in swollen target joint score (p < 0.001), tender target joint score (p < 0.002), and physician visual analog scale score (p < 0.001) after 4 weeks. Baseline MRI synovitis score was mean 5.08 (range 3-9) and was unchanged at followup in the whole group (p = 0.52) and between treatment groups (p = 0.43). MRI edema score (mean 4.46, range 0-29) in the total group was unchanged after 4 weeks (p = 0.13), whereas MRI erosion score increased in the total group from baseline, 17.88 (range 7-40), to 4 weeks, 18.25 (range 7-40) (p < 0.001). Neither US-Doppler color fraction (0.07) nor Resistive Index (RI) (p = 0.36) changed from baseline to 4 week followup. CONCLUSION: In contrast to the clinical evaluation, imaging measures of relevance for the estimation of inflammation, US-Doppler, US RI, MRI synovitis, and bone-marrow edema did not change 4 weeks after a single IA injection of either methylprednisolone or etanercept in the wrist. Within the same period, erosive progression in some patients suggested that joints with active disease may deteriorate within as little as 1 month, and that this development is not arrested by 1 injection. Given the small sample size of our study further studies are required to confirm our results.
17570371 Serum osteoprotegerin is increased and independently associated with coronary-artery ather 2007 Dec Osteoprotegerin (OPG), a soluble decoy receptor for receptor activator of nuclear factor kappaB ligand, is implicated in the pathogenesis of atherosclerosis. Patients with rheumatoid arthritis (RA) have inflammation and increased atherosclerosis. We examined the hypothesis that OPG concentrations are increased in patients with RA and are associated with coronary-artery atherosclerosis. Serum OPG concentrations were measured by ELISA and coronary-artery calcification by electron-beam computer tomography in 157 patients with RA and 87 control subjects. OPG concentrations were higher in patients with long-standing RA (n=67) [median (interquartile range)]: [1895 (1337-2847) pg/mL, and early RA (n=90): [1340 (1021-1652) pg/mL, than controls 1068 (692-1434) pg/mL; (p<0.001)]. In patients with RA, OPG concentrations were associated with erythrocyte sedimentation rate (p<0.001), homocysteine (p=0.001), disease duration (p=0.02), coronary calcium score (p=0.03), and cumulative dose of corticosteroids (p=0.04) after adjustment for age and sex. In patients with long-standing RA, OPG was associated with coronary-artery calcification independently of cardiovascular risk factors and disease activity [OR for every increase in 500 pg/mL of OPG=2.22 (1.43-3.34), p<0.001]. In conclusion, OPG concentrations are increased in patients with RA and are associated with inflammation. In patients with long-standing disease, OPG is independently associated with coronary-artery calcification.
18807103 Analyses of differential proteome of human synovial fibroblasts obtained from arthritis. 2009 Feb There is mounting evidence indicating that the synovial fibroblasts (SFs) contribute to the pathogenesis of rheumatoid arthritis (RA). The present study showed the differential proteins expression pattern of SFs from patients with RA or osteoarthritis (OA) and healthy control. Cellular proteins of cultured SFs were subjected to 2-DE and visualized by silver nitrate staining. A total of 49 spots that were statistically and differentially overexpressed in RA or OA in comparison to healthy ones were identified by MALDI-TOF-MS, and 25 proteins were successfully identified. Western blot was used to further verify some of the differential proteins. These proteins included enzymatic and structural proteins, signal transduction proteins, calcium binding protein, etc. From all of the identified proteins, a number of proteins have been implicated that involved in the healthy or pathological SFs function (e.g., S100A4, S100A10, cathepsin D) or that have potential diagnostic and prognostic value for RA (alpha-enolase and TPI) or that may be the new therapeutic targets (Annexin, SOD, PRX).
17433865 The pathogenesis of atherosclerosis in autoimmune rheumatic diseases: roles of inflammatio 2007 Mar As patients with autoimmune rheumatic diseases live longer due to improved therapies and preventive measures, death and disability from atherosclerosis, particularly myocardial infarcts, are increasing. The relative risks for atherosclerosis vary from approximately 1.6 in ankylosing spondylitis and psoriatic arthritis to 3.0 in rheumatoid arthritis (RA), and 6.0 in systemic lupus erythematosus (SLE). Increased risks are found when analyzed by atherosclerotic events, causes of death, or surrogate measures of atherosclerosis, such as carotid artery plaque, intimal-media thickness, or coronary artery calcification. At all ages among adults, atherosclerosis is increased in patients with SLE or RA compared to healthy controls. For example, in women with SLE under the age of 40 years, approximately 13% have carotid plaque compared to 2% of controls; over age 59 the percentages are 71 and 45, respectively. For patients with RA, prevalence is 7% under the age of 40 in patients compared to zero in controls; over 59 years the prevalences are 80% and 44%, respectively. In this review we will discuss the mechanisms involved as well as an overview of the natural history in pathobiology.
16918692 Genome-scale assessment of molecular pathology in systemic autoimmune diseases using micro 2006 Sep Systemic autoimmune rheumatic diseases are of complex aetiology, characterized by an intricate interplay of various factors. A myriad of genes lies behind the heterogeneous manifestations of these diseases, and the overexpression and repression of particular genes form a specific gene-expression profile (genetic fingerprints) that is characteristic to the given disease phenotype. Besides the description of various cell types by using gene-expression profiling, the data should be directly applicable to the design of individual therapeutic protocols for patients suffering from various autoimmune diseases. In this review, we summarize the gene-expression profile, various genetic signatures of different autoimmune diseases and give an overview on the possible interpretations of the data. The application of recent breakthroughs in high-throughput molecular profiling technologies, such as microarray technology has been the basis for a revolution in biomedical research, as well as diagnostics and pharmaceutical development. It is easy to envision a day when personalized medicine, which is the diagnosis and treatment of a given patient with agents and procedures tailored to that patient's genetics, physiology and pathology, will become the standard of care.
17355628 Rheumatoid peripheral blood phagocytes are primed for activation but have impaired Fc-medi 2007 Significant levels of circulating immune complexes (ICs) containing rheumatoid factors and immunoglobulin G in peripheral blood are a characteristic feature of rheumatoid arthritis (RA). ICs interact through Fc gamma receptors (Fc gammaR) to activate phagocytes in numerous inflammatory processes. The high concentration of neutrophils in synovial fluid during active phases of the disease, together with their destructive capacity, pose important questions as to their role in the pathogenesis of RA. Functional defects in RA or control peripheral blood neutrophil Fc gammaRs were examined with a specific Fc gammaR-mediated reactive oxygen species (ROS) assay. Heterologous cross-linking of Fc gammaRIIa and Fc gammaRIIIb on neutrophils resulted in a significantly decreased production of ROS by RA cells compared with controls matched for age and sex. However, expression and homologous ligation of receptors did not differ between these groups. These data suggest that neutrophil priming does occur before emigration into the joint and that blood neutrophils from patients with RA have a functional impairment in cooperative Fc gammaR-mediated ROS generation. This may account for the increased susceptibility to bacterial infection that arises in patients with severe disease.
16391893 Leflunomide/chloroquin combination therapy in rheumatoid arthritis: a pilot study. 2006 Jul The objective of this study was to assess the efficacy and tolerability of a combination of leflunomide (LEF) and chloroquin (ChL) in patients with rheumatoid arthritis (RA). Fifteen female RA patients (46-80 years, mean disease duration 100.7 months, ten patients RF+) were enrolled into this open trial. Patients were either treatment failures or partial responders to LEF (n=6) or ChL (n=9). At week 8 and 16, DAS28 and morning stiffness (MST) were evaluated. Moreover, safety was assessed by reporting of side effects, laboratory examinations, and blood pressure measurement. Baseline mean disease activity Index including a 28-joint count (DAS28) amounted to 5.61 and decreased to 4.54 at week 8 (p=0.023) and to 3.79 (p=0.00031) at week 16. MST remained unchanged. DAS28 values significantly decreased statistically in originally ChL-treated patients with additional LEF but did not in LEF patients with additional ChL (DAS28: 1.48; 2.29 vs 0.60; 0.87). Adverse reactions were observed in four patients. Three patients had to be withdrawn from the study. Combination therapy with LEF and ChL was effective and reasonably tolerated. The far higher treatment response could be observed in originally ChL-treated patients after initiation of LEF.
18506567 Safety profile of tacrolimus in patients with rheumatoid arthritis. 2008 Nov We assessed the safety of tacrolimus therapy for rheumatoid arthritis. Forty-two patients who started tacrolimus therapy between April 2005 and July 2006 were investigated retrospectively using data from their medical records up to June 2007. The cumulative treatment continuation rate was assessed by the Kaplan-Meier method. Fisher's exact test was used to compare gastrointestinal symptoms between different tacrolimus doses and between the presence and absence of each concomitant medication. The mean (+/-SD) observation period was 288 +/- 238 days. The cumulative treatment continuation rate was, respectively, 59.5% and 38.1% at 6 months and 1 year after the patients started treatment. Tacrolimus was discontinued in 28 patients, and was discontinued because of adverse reactions in 21 patients. Gastrointestinal symptoms were the most common adverse reactions (45.2% = 19/42 patients), followed by infections and hyperglycemia. Tacrolimus was discontinued in 9/19 patients with gastrointestinal symptoms, and was discontinued within 60 days of starting treatment in seven of them. Nausea and vomiting led to discontinuation in seven patients (within 60 days of starting treatment in six of them). The incidence of gastrointestinal symptoms was higher in patients receiving a daily dose >or=2 mg than in those receiving <2 mg/day. During treatment of rheumatoid arthritis by oral tacrolimus therapy, gastrointestinal symptoms were common, early, and dose-dependent. However, these symptoms were not severe and did not cause any serious safety problems.
18349743 Genetic variants that predict response to anti-tumor necrosis factor therapy in rheumatoid 2008 Mar PURPOSE OF REVIEW: Tumor necrosis factor alpha (TNF) inhibitors are a mainstay of treatment in rheumatoid arthritis, yet there are no effective clinical or biomarker predictors of which patients will respond. Here we review genetic association studies conducted to search for DNA biomarkers of response to anti-TNF therapy. RECENT FINDINGS: The entirety of genetic association studies to date that focus on response to anti-TNF therapy has been limited to a small number of genetic variants within a few candidate genes (primarily within the major histocompatibility complex region). Moreover, these studies have been conducted in a relatively small number of rheumatoid arthritis patients (approximately 1000 patients across all studies combined). From these studies, no single genetic factor is associated unequivocally with treatment response, although some studies suggest that alleles within the major histocompatibility complex may influence response. SUMMARY: Additional studies are required to investigate the genetic basis of response to anti-TNF therapy. These studies should include an unbiased search of DNA variation across the human genome--now feasible through cost-effective genome-wide association studies--and be conducted in large patient collections powered to detect modest effect sizes.
18234999 Corneal involvement in rheumatoid arthritis: an in vivo confocal study. 2008 Feb PURPOSE: To analyze the in vivo morphology of corneal cells and nerves in patients with rheumatoid arthritis (RA), with or without secondary Sjögren's syndrome (SSII), and to investigate the correlations between corneal alterations and RA activity. METHODS: Fifty patients with RA and 30 age- and gender-matched control subjects were studied. SSII was diagnosed according to the American-European Consensus Group criteria, and RA activity was evaluated by the Lansbury index (LI). Confocal microscopy was used to investigate corneal thickness, the number of epithelial and stromal cells, and keratocyte hyperreflectivity. In addition, the sub-basal plexus was assessed for the number, tortuosity, and reflectivity of the nerve fibers and the presence of beadlike formations. RESULTS: Sixteen percent of patients with RA also had SSII. Between the SSII and non-SSII groups, no significant differences were found in the LI or in the clinical and confocal variables. Significant differences were present between patients with RA and control subjects for all the variables studied except nerve reflectivity. In patients with RA with and without SSII, LI correlated significantly with the number of beadlike formations and the number of hyperreflective, activated keratocytes. CONCLUSIONS: Confocal microscopy of patients with RA showed several changes in corneal cells and nerves. The number of beadlike formations and the number of activated keratocytes could be interpreted as confocal signs of ocular surface disease activity. These correlations with the index of systemic disease activity, LI, may provide insight regarding the pathogenic mechanisms of dry eye in patients with RA.
16806231 Inflammatory suppression rapidly attenuates microvascular dysfunction in rheumatoid arthri 2007 Jun Rheumatoid arthritis (RA) is associated with greater risk of cardiovascular morbidity and mortality, the inflammatory component of RA being strongly linked to this excess risk. Endothelial dysfunction is linked to atherosclerosis and has been demonstrated in larger vessels in RA. In this pilot study, we determined for the first time whether skin microvascular function was impaired in patients with active RA and also determined its response to anti-inflammatory treatment. This was assessed non-invasively using laser Doppler imaging combined with iontophoresis of the vasodilators acetylcholine (ACh, endothelium dependent) and sodium nitroprusside (SNP, endothelium independent) to the forearm. Eight RA patients admitted for acute flare-ups were assessed before and following anti-inflammatory treatment. Standard laboratory indices were obtained along with pain perception (VAS). A control group of eight subjects was included for baseline comparison. Compared to this group, vascular function was substantially and significantly (P<0.00001) lower in RA patients. Following treatment, as CRP and VAS decreased, vascular function improved for both ACh (P<0.00001) and SNP (P=0.001), this improvement being significantly greater for ACh (P<0.001). Vascular dysfunction is evident in RA patients, even at the level of the cutaneous microcirculation, but improves as inflammation regresses. Assessment of cutaneous vascular function may be a useful, non-invasive surrogate indicator of vascular risk in RA, inclusive of myocardial microvascular abnormalities.
18980958 Polymyalgia rheumatica can be distinguished from late onset rheumatoid arthritis at baseli 2009 Feb OBJECTIVE: To describe the pattern of arthropathy and HLA-DRB1 alleles associated with PMR in order to develop a diagnostic algorithm that could help distinguish PMR and RF-negative (RF -ve) late-onset RA (LO-RA) at presentation. METHODS: This was a prospective study of all patients presenting with PMR or LO-RA over a 10-yr period to one physician. Demographic, clinical and laboratory data were collected at presentation and during a minimum of 5 yrs of follow-up. The accuracy of the initial diagnosis was systematically reviewed. RESULTS: One hundred and forty-two patients with LO-RA, 147 with PMR and 42 with PMR + TA were studied. Peripheral synovitis was observed in 23% of the PMR patients. In comparison with RF -ve LO-RA, PMR patients were younger (P < 0.001), myalgia more frequent [100 vs 16% (P < 0.001)] and arthritis of PIP, MCP and wrist were less frequent (P < 0.001). The combination of wrist + MCP/PIP or wrist + PIP + MCP were highly suggestive of RF -ve LO-RA (P < 0.001). HLA-DRB1*0101/0102 and *0401 were significantly increased in PMR patients compared with healthy controls. Plasma viscosity and arthritis in the wrist, in combination with at least one MCP or PIP joint at disease onset, were predictive of whether a non-erosive RF -ve patient would ultimately be diagnosed as having RF -ve LO-RA or PMR (+/-/arthritis). CONCLUSION: Our longitudinal follow-up data were consistent with RF -ve LO-RA being a separate disease entity to PMR despite some phenotypic and immunogenetic similarities at disease onset. A diagnostic algorithm was derived using baseline clinical features to predict the final diagnosis of RF -ve, non-erosive patients.
17611988 Clinical evaluation of anti-mutated citrullinated vimentin by ELISA in rheumatoid arthriti 2007 Aug OBJECTIVE: Anti-cyclic citrullinated peptide (CCP) antibodies have emerged as sensitive and specific serological markers of rheumatoid arthritis (RA). However, antibodies to several other citrulline-containing proteins, including citrullinated fibrin and vimentin, have been detected in patients with RA, suggesting that citrulline is an essential constituent of autoantigens for RA-specific autoantibodies. We examined the diagnostic performance of the newly developed anti-mutated citrullinated vimentin (MCV) antibody assay. METHODS: Concentrations of anti-MCV, anti-CCP2, and rheumatoid factors (RF) were determined in the sera of 237 individuals: 119 patients with RA and 118 controls, including patients with other rheumatic diseases and healthy subjects. Diagnostic properties were compared by receiver-operating characteristic curve analysis. RESULTS: Using manufacturer's recommended cutoff values, sensitivity and specificity of anti-MCV antibodies were 75.6% and 91.5% in RA, compared to 66.4% and 98.3% for anti-CCP2. Introducing cutoff values to obtain the same 95% specificity resulted in decreased sensitivity of the anti-MCV test (69.7%) and increased sensitivity of the anti-CCP2 test (74.8%). At optimal cutoff levels, 29.4% of IgM RF-negative cases as well as 13.3% of anti-CCP2-negative cases in the RA group were anti-MCV-positive. Double-positivity for anti-MCV and anti-CCP2 provided 98.3% specificity with 97.5% positive predictive value in RA. CONCLUSION: Overall, the performance of the novel anti-MCV ELISA for the diagnosis of RA is similar to that of the anti-CCP2 test [area under the curve 0.853 (95% CI 0.801-0.905) vs 0.910 (95% CI 0.873-0.946); p not significant]. As the diagnostic spectrum of the anti-MCV assay is somewhat different from that of anti-CCP2, the combined application of the 2 assays can improve the laboratory diagnostics of RA.
18162190 High levels of the proNGF peptides LIP1 and LIP2 in the serum and synovial fluid of rheuma 2008 Feb The proNGF peptides LIP1 and LIP2 display multiple biological and physiological properties several of which share common features with the nerve growth factor (NGF). The objective of this study was firstly to demonstrate the presence of these peptides in the human sera and secondly to provide evidence for their involvement in inflammatory diseases. Their levels measured by specific enzyme-linked immunosorbent assays (ELISA) were found to be more than 10-fold higher in sera of patients with rheumatoid arthritis (RA), as compared to healthy controls. High levels of LIP1 and LIP2 were also detected in the synovial fluid (SF) of RA patients. These results provide first evidence for a cytokine-like role of the LIP1 and LIP2 peptides.
17572650 How good is to switch between biologics? A systematic review of the literature. 2007 Apr Despite the biological rationale for switching between TNF-antagonists, there is not a definitive answer from a clinical point of view. METHODS: We performed a systematic review. The strategy for the literature search included synonyms for the active drugs, trade names, and different synonyms for biologic therapies, plus the words "switch" or "switching", limited to studies in humans. The time limit was March 1st 2007. From 256 initial hits in Medline and Embase, plus 13 abstracts from rheumatology meetings, we finally included 33 studies. RESULTS AND DISCUSSION: The most frequently died switches are those between etanercept and infliximab. The mean number of patients studied per type of switch was 126. There are, apart from retrospective observational studies and cases series, 5 prospective cohorts from biologic registries, 1 randomised open-label clinical trial and 1 phase IV clinical trial, all seven of which are of moderate to good quality. There results are promising but not excellent. Any switch, especially those between monoclonal antibodies, have an effect size that is usually lower than that of a first biologic. When the switch is due to an adverse event with the first TNF-antagonist, however, the response rate of the second one is high. Perhaps the best alternative when a first TNF-antagonist fails is to start a different type of biologic, and leave the switch to another TNF-antagonist in the case of adverse event to the previous one.
18289674 Observations favouring the occurrence of local production and marked effects of bombesin/g 2008 Apr We have previously shown that levels of the neuropeptides substance P (SP) and bombesin/gastrin-releasing peptide (BN/GRP) in blood and synovial fluid correlate with levels of pro-inflammatory cytokines in patients with rheumatoid arthritis (RA). It is well-established that SP is present in nerve endings in the synovium whilst the source of BN/GRP in human joints is completely unknown. Nor is it known whether GRP-receptors (GRP-R) are present in human synovial tissue. This study aimed to investigate the expression pattern of SP, BN/GRP and their receptors (NK-1R and GRP-R) in synovial tissue. Synovial tissue specimens from patients with RA or osteoarthritis (OA) were processed for immunohistochemistry, in situ hybridisation and ELISA. The results show the presence of BN/GRP, but not SP, in cells in the synovial tissue at both the protein and mRNA level. We did not find immunoreactive BN/GRP in nerve structures. NK-1R and GRP-R were also expressed at both protein and mRNA levels in cells associated with blood vessels and cells in the interstitial tissue. ELISA analyses revealed both SP and BN/GRP to be present in synovial tissue extracts and that synovial levels of SP were higher in RA patients than those with OA. Our results indicate that BN/GRP is produced by non-neuronal cells in the synovial tissue. Furthermore, both BN/GRP and SP may exert their effects on the synovial tissue through the respective receptors. These results suggest that BN/GRP and SP may modulate inflammation and vascular events, and possibly healing processes in the synovium. Finally, nerves should not be considered as the source of BN/GRP in synovial tissue although this peptide is presumably intimately involved functionally in synovial tissue, a previously unrecognised fact.
18398940 Validation of self-report of rheumatoid arthritis and systemic lupus erythematosus: The Wo 2008 May OBJECTIVE: The Women's Health Initiative (WHI), initiated in 1993, enrolled 161,808 postmenopausal women aged 50-79 years and followed them with annual questionnaires for 8 years in order to study major causes of morbidity and mortality. Our objective was to determine the most effective and efficient means to validate self-reported rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) in the WHI. METHODS: Data from 2 of 40 WHI clinical centers were used. Of these 7443 women, 643 self-reported RA and 106 self-reported SLE. Research coordinators contacted these women using mailers and telephone calls to obtain medical record releases and a Connective Tissue Screening Questionnaire (CSQ). Medical records were obtained on 286 self-reported RA and 34 self-reported SLE and reviewed by 3 rheumatologists blind to the self-reported diagnoses. Sensitivity, specificity, and the kappa statistic were computed to evaluate the level of agreement between self-report and chart review. RESULTS: Self-reported RA was accurate only 14.7% (42/286 cases) of the time. Coupling the self-report to medication data improved the positive predictive value (PPV; 62.2%) and kappa (0.53), suggesting a moderate agreement to chart review. Self-reported SLE was accurate only 11.8% (4/34 cases) of the time. Coupling the self-report to medication data improved the PPV (40.0%) and kappa (0.44), suggesting a moderate agreement to chart review. The CSQ was inferior to using medication data but was substantially better than self-report alone. CONCLUSION: The performance of disease self-report coupled with medication history in validating RA and SLE was very good and should obviate the need for time-consuming medical record reviews.
17659935 Characterization of valvular heart disease in rheumatoid arthritis by transesophageal echo 2007 Aug 1 Valvular heart disease (VHD) associated with rheumatoid arthritis (RA) has not been well characterized and its clinical predictors are undefined. Therefore, 34 volunteers with RA with a mean age of 50 +/- 10 years underwent clinical evaluation and transesophageal echocardiography. Findings on transesophageal echocardiography were compared with those of 34 gender-matched healthy volunteers with a mean age of 42 +/- 6 years. Twenty patients (59%) had mainly (97%) left-sided VHD (valve nodules in 11, 32%; valve thickening in 18, 53%; valve regurgitation in 7, 21%; and valve stenosis in 1, 3%) compared with 5 controls (15%; [nodules in 1, 3%; thickening in 4, 12%; and regurgitation in 1, 3%; p < or =0.05 for all vs patients). Valve nodules were generally single and small (4 to 12 mm); were oval with regular borders and had homogenous echocardiographic reflectance; were typically located at the leaflets' basal or mid portions; and equally affected the aortic and mitral valves. Valve thickening was equally diffuse or localized; when localized affected any leaflet portion; was usually mild (89%); involved similarly the mitral and aortic valves (47% and 32%, respectively); and rarely (6%) involved the annulus and subvalvular apparatus. Valve regurgitation manifested as mild aortic regurgitation in 4 patients, moderate mitral regurgitation in 4 patients, and moderate tricuspid regurgitation in 1 patient. Mitral and aortic valve stenoses occurred in 1 patient (3%). No correlation was found between VHD and duration, activity, severity, pattern of onset and course, extra-articular disease, serology, or therapy of RA. In conclusion, RA-associated VHD is common, valve nodules and thickening are its distinctive features, and it is not associated with clinical variables of RA.
17626700 A multicenter, randomized, open study to evaluate the impact of an electronic data capture 2007 Aug OBJECTIVE: To examine the impact of an electronic data capture system on patient satisfaction and patient-physician interactions in a rheumatology clinical setting. STUDY DESIGN: In this multicenter study, 1079 patients with rheumatoid arthritis completed questionnaires quarterly about their health and satisfaction with care using a computer. At 6 months, 901 eligible patients were randomized 2:1 to receive or not to receive graphical summarized health information or Health Tracker (HT) reports. Data collected at each visit included patient satisfaction with care; patient-physician interaction assessments; a 56-joint self-assessment for patients; a 28-joint assessment for physicians; patient pain, fatigue, and global assessments (visual analogue scale, physician global assessment, Health Assessment Questionnaire, and Short Form-12) all of which were cumulatively recorded in the HT report. RESULTS: Patient demographics at baseline were similar between groups. Changes from baseline to 1 year showed that patients in the HT-viewers group were significantly more satisfied with their care (p < 0.001) than those in the HT-nonviewers group (p = 0.131). Physicians reported improved interactions with patients at 1 year in both the HT-viewers (p < 0.001) and HT-nonviewers groups (p = 0.002); however, the improvement was significantly larger for the HT-viewers group than for the HT-nonviewers group (p < 0.001). Adverse events were comparable between groups. CONCLUSIONS: Patient access to systematically collected patient data reports promoted self-involvement and improved patient satisfaction and patient-physician interactions more in the HT-viewers than in HT-nonviewers groups at 1 year (p < 0.001). This was an open, observational study; no formal hypothesis testing was conducted. The HT system was not validated and some bias may have existed with respect to patient comfort level with a computer, user error, and timing of data entry of the physicians' assessments.
16899502 Autoantibodies, metalloproteinases and bone markers in rheumatoid arthritis patients are u 2007 Mar OBJECTIVES: To identify biochemical, immunological and bone markers as predictors of rheumatoid arthritis (RA) patients' responses to infliximab. METHODS: A total of 76 patients with active RA (American College of Rheumatology criteria), refractory to disease-modifying anti-rheumatic drugs, including methotrexate, received infliximab (3 mg/kg) infusions at weeks 0, 2, 6, and then every 8 weeks in combination with methotrexate or leflunomide. At week 14, infliximab efficacy was evaluated using disease activity score (DAS)28. A serum sample, collected just before starting infliximab, was tested by ELISA (unless stated otherwise) for the following immunological markers: rheumatoid factor by agglutination and ELISA (IgA, IgG and IgM isotypes); anti-cyclic citrullinated protein; autoantibodies recognizing calpastatin domain I and its 27 C-terminal fragment, glucose-6-phosphate isomerase, alpha-enolase; anti-keratin and anti-perinuclear factor antibodies (immunofluorescence); biochemical markers: C-reactive protein (nephelometry), metalloproteinase-1 and -3, tissue inhibitors of metalloproteinases-1 and -2, antioxidants (vitamins A and E; selenium); bone resorption markers: pyridinoline, deoxypyridinoline, osteoprotegerin, soluble receptor activator of nuclear factor-kappaB ligand, cartilage oligomeric matrix protein. Each parameter's predictive value of the response to infliximab was analysed using Fisher's exact, Mann-Whitney and chi-square tests. Hierarchical clustering was performed with The Institute for Genomic Research (TIGR) multiple experiment viewer software. RESULTS: Good, moderate and non-responder rates were 6.5, 61.8 and 31.5%, respectively. No significant difference was observed between responders and non-responders, regardless of the serum parameters considered. Analysis of dichotomous or continuous variables failed to identify markers predictive of a good or poor response to infliximab. CONCLUSION: The search for soluble markers in RA patients' sera likely to predict response to infliximab because of their involvement in RA pathogenesis seems disappointing. However, because of the limited power to detect smaller differences in biomarkers, the present study is a preliminary exploratory analysis.