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ID PMID Title PublicationDate abstract
20505626 [Sexual function in rheumatic diseases]. 2010 Jan Sexual function is closely related to satisfactory quality of life. The sexual activity has an impact in the sexual satisfaction of patient, several aspects of personal life and in their relationships. Systemic autoimmune diseases affect various organs and systems and they can determine sexual dysfunction in patients, particularly with: rheumatoid arthritis, spondyloarthropathies, systemic lupus erythematosus, systemic sclerosis, Sjögren syndrome, vasculitis and idiopathic inflammatory myopathies. Manuscripts describing sexual function in these diseases, mainly with large population, are scarce. Sexual dysfunction in females and males with rheumatic diseases is multifactorial due to chronic disease aspects, disease activity and drugs. A multidisciplinary approach is essential in order to offer preventive measures for these patients. The authors did a literature review based on Medline, Lilacs and Pubmed data using the keywords: sexual function, sexuality, reproductive health and rheumatic diseases.
20037209 Genetic factors associated with rheumatoid arthritis and systemic vasculitis: Evaluation o 2009 Immune and inflammatory response activation is a common feature of connective tissue diseases and systemic vasculitis. The aim of our study was to evaluate the possible involvement of TNFalpha c.-308A > G, IL-10 c.-1082A > G, uteroglobin c.38A > G, TGFbeta 1 c.869C > T and NFkappaB2 c.-1837T > C gene polymorphisms in susceptibility to connective tissue diseases. Our study cohort included 68 unrelated patients affected by rheumatoid arthritis (RA) (37 patients) and ANCA-positive [micropolyangiitis (mPA) 17 patients] or ANCA-negative systemic vasculitis [including 8 patients with Henoch-Schönlein purpura (HSP) and 6 patients with mixed cryoglobulinaemia (MC)] as well as 98 control subjects. Allele frequency analysis of uteroglobin c.38G > A polymorphism showed a significant increase in the c.38A allele in patients (p= 0.002). Genotype frequency analysis of uteroglobin and NF-kappaB2 gene polymorphisms in patients showed an increase in c.38GA and c.38AA genotypes in the uteroglobin gene (p=0.02) coupled with an increase in homozygous c.-1837CC in the NF-kappaB2 gene (p=0.02). Our data suggest that genetic variation in UG and NF-kappaB2 pathways could have effects in connective tissue disease susceptibility.
21119718 Current view of glucocorticoid co-therapy with DMARDs in rheumatoid arthritis. 2010 Dec Glucocorticoids are widely used anti-inflammatory and immunosuppressive drugs for rheumatoid arthritis (RA). The disease-modifying potential of low to medium doses of glucocorticoids has been reconfirmed in the past decade, and co-administration of DMARDs and glucocorticoids has become standard in many treatment protocols, especially those for early disease stages but also for long-standing RA. The glucocorticoid regimens used range from continuous low doses to intermittent high doses. Studies of the rationale for and clinical use of glucocorticoids as co-therapy with DMARDs in RA have shown that this approach has a place in modern (tight control) treatment strategies, and that glucocorticoid co-therapy has disease-modifying effects during the first 2 years of treatment in patients with early RA. Furthermore, medium and high doses of glucocorticoids are useful for bridging the interval between initiation of DMARDs and onset of their therapeutic effect. Intra-articular glucocorticoids give good local control and have been used in tight control strategies. New glucocorticoid compounds are becoming available for clinical use that might have an enhanced risk:benefit ratio. Better monitoring of glucocorticoid use will also improve this ratio, and help to allay both patient and rheumatologist concerns about treatment-related adverse effects.
20004775 Autoinflammation: the prominent role of IL-1 in monogenic autoinflammatory diseases and im 2009 Dec The discovery of the genetic causes of a rare group of immune-mediated inflammatory conditions that mimic infections and allergic conditions in their clinical presentation and the molecular understanding of the function of the mutated molecules in these diseases has led to a revolution in our understanding of the pathogenesis of systemic and local inflammation. The proteins mutated in a number of these so-called autoinflammatory diseases are part of, or regulate the activity of, intracellular molecular complexes, the inflammasomes, that sense "danger" to the body and coordinate an initial immune response. Our understanding of specific triggers of the inflammasomes, coupled with the recognition that inflammasomes are critical for activation of the proinflammatory cytokine IL-1, has provided a rational and very effective target in the treatment of a number of these rare autoinflammatory diseases. In addition, the ongoing discovery of the role of inflammasomes and IL-1 activation and secretion in a number of genetically complex disorders have fundamentally changed our view of disease pathogenesis in a growing number of disorders that were heretofore not even thought of as "immunologic" diseases.
21045991 Distal radius hemiarthroplasty combined with proximal row carpectomy: case report. 2010 Severe wrist arthritis is most commonly treated by complete wrist arthrodesis, which provides predictable pain relief but the loss of motion may reduce ease of function. In selected patients, motion preserving surgical options, including limited intercarpal fusion, proximal row carpectomy (PRC), and total wrist arthroplasty (TWA) are considered. However, limited fusion and PRC are typically possible only in less severe cases in which there are some articular surfaces showing minimal degeneration that can be retained. TWA is an option for patients who have lower activity demands and specific needs or desires to maintain some wrist motion. Recent utility and decision analysis studies demonstrate that arthroplasty is associated with higher qualify adjusted life year (QALY) than arthrodesis in patients with rheumatoid arthritis. Despite these positive aspects of TWA, the procedure is not as widely accepted as hip, knee, or shoulder arthroplasty. Early implants had problems related to both materials and design, with breakage, loosening and joint imbalance being common complications. Newer generation implants are improved with more predictable early function, less joint imbalance, and rare breakage, but distal component loosening remains a substantial problem. Thus, patients with poor bone stock and those with high activity demands are typically not candidates for TWA, and all patients are advised to restrict activities to reduce the risk of implant loosening. A new motion preserving procedure has recently been used at our institution in selected patients with severe arthritis who do not qualify for TWA but request an alternative to complete wrist fusion. In this procedure, a distal radius implant arthroplasty is combined with a PRC. The distal radius component of a Universal 2 (UNI 2) total wrist arthroplasty system (Integra life Sciences, Plainsboro, NJ) is used. To our knowledge, there have been no previous publications on this technique. We report our first two cases which have shown a satisfactory early outcome for pain relief and functional wrist motion.
20363159 Reverse shoulder arthroplasty in patients with rheumatoid arthritis. 2010 Oct BACKGROUND: The purpose of this study was to describe the pathoanatomy of patients diagnosed with rheumatoid arthritis and rotator cuff deficiency and report their outcomes following reverse shoulder arthroplasty. METHODS: Twenty-one shoulders were evaluated prospectively. Nine had no prior surgery, 9 had a failed rotator cuff repair, and 3 had a failed arthroplasty. Patients were followed for a minimum of 2 years (average, 36 months). All patients had preoperative radiographs and 19 shoulders had an MRI or CT available for evaluation of muscular and bony deficiency. Radiographs at most recent follow-up were evaluated for loosening and scapular notching. RESULTS: All outcome measures improved significantly: ASES scores improved from 28 preoperatively to 82 postoperatively (P < .0001); SST scores improved from 1 to 7 (P < .0001); VAS pain scores improved from 7 to 1 (P < .0001); VAS function scores improved from 3 to 6 (P=.0058); elevation improved from 52° to 126° (P < .0001); abduction improved from 55° to 116° (P=.0002); external rotation improved from 19° to 33° (P=.02); and internal rotation improved from S1 to L4 (P=.02). Twelve patients rated their outcome as excellent, 6 as good, 2 as satisfactory, and 1 as unsatisfactory. Severe glenoid erosion was seen in 10 of the shoulders and 5 of the defects required structural grafting. Three patients (14%) sustained a complication that required reoperation: 2 for infection and 1 for periprosthetic fracture. CONCLUSIONS: In patients with rheumatoid arthritis and rotator cuff deficiency, reverse shoulder arthroplasty can provide improvement in function and decreased pain.
20634036 No clear advantage to use of wound drains after unilateral total knee arthroplasty: a pros 2011 Jun We conducted a prospective randomized, controlled trial in 100 patients to compare the postoperative use of wound drains with the use of no drains in patients who underwent unilateral primary total knee arthroplasty to determine differences in blood loss, range of motion, wound healing, complications (deep vein thrombosis, wound infection), and need for blood transfusions. The patients, who underwent surgery between February 2006 and February 2007, were randomly divided into 2 groups of 50 each: group A, treated without a drain, and group B, treated with a drain. The between-group difference in total blood loss was significant: 535 ± 295 mL in group A and 853 ± 331 mL in group B. Group A needed comparatively less blood transfused than group B did. Differences in wound infection, incidence of deep vein thrombosis, and range of motion were not statistically significant between groups. We found no clear advantage to the use of wound drains in unilateral total knee arthroplasty.
19671814 Proposal for levels of evidence schema for validation of a soluble biomarker reflecting da 2009 Aug OBJECTIVE: At OMERACT 8 a framework for levels of evidence was proposed for the validation of biomarkers as surrogate outcome measures. We aimed to adapt this scheme in order to apply it in the setting of soluble biomarkers proposed to replace the measurement of damage endpoints in rheumatoid arthritis (RA), psoriatic arthritis (PsA), and ankylosing spondylitis (AS). We also aimed to generate consensus on minimum standards for the design of longitudinal studies aimed at validating biomarkers. METHODS: Before the meeting, the Soluble Biomarker Working Group prepared a preliminary framework and discussed various models for association and prediction related to the statistical strength domain. In addition, 3 Delphi exercises addressing longitudinal study design for RA, PsA, and AS were conducted within the working group and members of the Assessments in SpondyloArthritis International Society (ASAS) and the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA). This formed the basis for discussions among OMERACT 9 participants. RESULTS: The proposed framework was accepted by consensus. In the study design domain a requirement for both prospective observational studies and randomized controlled trials (RCT) in different drug classes was noted. A template for determining the level of statistical strength was proposed. The addition of a new domain on biomarker assay performance was considered essential, and participants suggested that for any biomarker this domain should be addressed first, i.e., before starting clinical validation studies. Participants agreed on most elements of a longitudinal study design template. Where consensus was lacking the working group has drafted solutions that constitute a basis for prospective validation studies. CONCLUSION: The OMERACT 9 Soluble Biomarker Group has successfully formulated a levels of evidence scheme and a study design template that will provide guidance to conduct validation studies in the setting of soluble biomarkers proposed to replace the measurement of damage endpoints in RA, PsA, and AS.
21284345 Oxidative stress and enzymatic antioxidant status in rheumatoid arthritis: a case control 2010 Nov BACKGROUND AND OBJECTIVES: Rheumatoid arthritis (RA) is a chronic multisystem disease of unknown cause. Formation of reactive oxygen species and lipid peroxides as a result of disease activity may play an important role. Oxidative stress and decreased antioxidant status are the hallmarks in patients of RA as observed in recent years. The objectives of the study was to determine oxidative stress by measuring malondialdehyde and enzymatic antioxidant status by estimating superoxide dismutase and glutathione reductase in patients of RA and then comparing with healthy individuals. MATERIALS AND METHODS: The present study comprises of 40 RA cases who were clinically diagnosed and confirmed by laboratory tests, attending KLE Society's Dr. Prabhakar Kore Hospital and Research Centre, Belgaum. Southern India attached to J. N. Medical College. between September 2007 to August 2008. All the patients were in the age group of 40-60 years including both the sexes. Biochemical parameters like malondialdehyde, enzymatic antioxidants like superoxide dismutase and glutathione reductase were estimated in cases (40) and controls (40). RESULTS: The mean level of blood malondialdehyde (in nmol/ml) in controls was 6.19 +/- 0.96 and 11.48 +/- 0.76 in cases. The mean level of superoxide dismutase (IU/g of Hb) in controls was 948.32 +/- 99.88 and 443.68 +/- 111.69 in the cases. The mean glutathione reductase level (in IU/g of Hb) in controls was 8.91 +/- 1.04 and 2.96 +/- 0.79 in the cases. CONCLUSIONS: This study revealed that there was an increased oxidative stress and a decreased antioxidant defense in patients with rheumatoid arthritis.
19280938 [Biological agents]. 2009 Mar There are two types of biological agents for the treatment of rheumatoid arthritis (RA); monoclonal antibodies and recombinant proteins. Among the latter, etanercept, a recombinant fusion protein of soluble TNF receptor and IgG was approved in 2005 in Japan. The post-marketing surveillance of 13,894 RA patients revealed the efficacy and safety profiles of etanercept in the Japanese population, as well as overseas studies. Abatacept, a recombinant fusion protein of CTLA4 and IgG, is another biological agent for RA. Two clinical trials disclosed the efficacy of abatacept for difficult-to-treat patients: the AIM for MTX-resistant cases and the ATTAIN for patients who are resistant to anti-TNF. The ATTEST trial suggested abatacept might have more acceptable safety profile than infliximab. These biologics are also promising for the treatment of RA for not only relieving clinical symptoms and signs but retarding structural damage.
19852746 Rheumatoid arthritis and systemic lupus erythematosus as immune complex diseases. 2009 Rheumatoid factors are 9s IgM autoantibodies directed against the hinge regions of 7s IgG's that have been changed consequent to their encounter with a foreign antigen, such as those produced by oral bacteria. Occasionally self-aggregating 7s IgG's serve this function. When these complexes are taken up by phagocytes in the joint, they form the "RA cell," a cell analogous to the LE cell of Hargraves. The circulating complexes, which activate complement cascades in the joint, are not specific for RA, being found in other rheumatic and autoimmune diseases as well as having a low prevalence in the normal population. Recently, other antigens resulting in autoimmune complex formation with greater specificity for RA have been described. These antibodies, known as anti-cyclic citrullinated peptide (anti-CCP) antibodies recognize citrullinated protein residues, which are present as antigenic determinants in patients with RA. This is in contrast to systemic lupus erythematosus (SLE), another autoimmune disease characterized by immune complexes in the systemic circulation. In the case of SLE, 7s IgG's directed against several nuclear antigens localize mainly in the kidneys and blood vessels. They also produce cerebral and pulmonary disease by activating complement systemically. Genetic defects in the complement cascade associated with SLE result in inadequate clearance of immune complexes as well as apoptotic blebs containing autoantigens.
20665032 Nicotine inhibits tumor necrosis factor-α induced IL-6 and IL-8 secretion in fibroblast-l 2012 Jan It was recently demonstrated that the cholinergic anti-inflammatory pathway can modulate host inflammatory responses via cholinergic mediators or via electrical stimulation of the vagus nerve. Here, we investigated whether nicotine, a selective cholinergic agonist, plays any anti-inflammatory role in rheumatoid arthritis fibroblast-like synoviocytes (FLS). We observed that low concentrations (0.1-100 μM) of nicotine did not affect FLS viability in lactate dehydrogenase release test or the MTT assay. Nicotine at concentrations of 0.1-10 μM dose reduced the protein and mRNA expression of IL-6 and IL-8 induced by tumor necrosis factor-α (TNFα). Nicotine also inhibited nuclear factor (NF)-κB (p65) translocation from the cytoplasm to the nucleus, based on Western blotting and immunocytochemical analysis. In conclusion, nicotine can inhibit the TNFα dependant inflammatory pathway in synoviocytes by suppressing the activation of the NF-κB pathway.
19884493 Adoptive therapy with redirected primary regulatory T cells results in antigen-specific su 2009 Nov 10 Regulatory T cells (Tregs) can suppress a wide range of immune cells, making them an ideal candidate for the treatment of autoimmunity. The potential clinical translation of targeted therapy with antigen-specific Tregs is hampered by the difficulties of isolating rare specificities from the natural polyclonal T cell repertoire. Moreover, the initiating antigen is often unknown in autoimmune disease. Here we tested the ability of antigen-specific Tregs generated by retroviral gene transfer to ameliorate arthritis through linked suppression and therefore without cognate recognition of the disease-initiating antigen. We explored two distinct strategies: T cell receptor (TCR) gene transfer into purified CD4+CD25+ T cells was used to redirect the specificity of naturally occurring Tregs; and co-transfer of FoxP3 and TCR genes served to convert conventional CD4(+) T cells into antigen-specific regulators. Following adoptive transfer into recipient mice, the gene-modified T cells engrafted efficiently and retained TCR and FoxP3 expression. Using an established arthritis model, we demonstrate antigen-driven accumulation of the gene modified T cells at the site of joint inflammation, which resulted in a local reduction in the number of inflammatory Th17 cells and a significant decrease in arthritic bone destruction. Together, we describe a robust strategy to rapidly generate antigen-specific regulatory T cells capable of highly targeted inhibition of tissue damage in the absence of systemic immune suppression. This opens the possibility to target Tregs to tissue-specific antigens for the treatment of autoimmune tissue damage without the knowledge of the disease-causing autoantigens recognized by pathogenic T cells.
19715572 Rituximab therapy reduces activated B cells in both the peripheral blood and bone marrow o 2009 INTRODUCTION: Bone marrow (BM) is an immunologically privileged site where activated autoantibody-producing B cells may survive for prolonged periods. We investigated the effect of rituximab (anti-CD20 mAb) in peripheral blood (PB) and BM B-cell and T-cell populations in active rheumatoid arthritis (RA) patients. METHODS: Active RA patients received rituximab (1,000 mg) on days 1 and 15. PB (n = 11) and BM (n = 8) aspirates were collected at baseline and at 3 months. We assessed B-cell and T-cell populations using triple-color flow cytometry. RESULTS: Rituximab therapy decreased PB (from a mean 2% to 0.9%, P = 0.022) but not BM (from 4.6% to 3.8%, P = 0.273) CD19+ B cells, associated with a significant reduction in the activated CD19+HLA-DR+ subset both in PB (from 55% to 19%, P = 0.007) and in BM (from 68% to 19%, P = 0.007). Response to rituximab was preceded by a significant decrease in PB and BM CD19+CD27+ memory B cells (P = 0.022). These effects were specific to rituximab since anti-TNF therapy did not reduce total or activated B cells. Rituximab therapy did not alter the number of activated CD4+HLA-DR+ and CD4+CD25+ T cells. CONCLUSIONS: Rituximab therapy preferentially depletes activated CD19+HLA-DR+ B cells in the PB and BM of active RA patients. Clinical response to rituximab is associated with depletion of CD19+CD27+ memory B cells in PB and BM of RA patients.
19585382 Health status and perception of pain: a comparative study between female patients with han 2009 OBJECTIVE: Osteoarthritis (OA) is the most frequent rheumatic joint disease and its occurrence is growing due to prolonged life expectancy and an increasing number of elderly individuals in the population. The main objective of this study was to compare the burden of disease, assessed by measures of pain and health-related quality of life (HRQoL), between female patients with hand osteoarthritis (HOA) and rheumatoid arthritis (RA). METHODS: One hundred and ninety female HOA patients were compared with 194 female RA patients of the same age. HRQoL was measured with the Arthritis Impact Measurement 2 Scale (Aims2), the 36-item Short-Form Health Survey (SF-36) and its preference-based single index measure SF-6D, the Health Assessment Questionnaire (HAQ), the modified HAQ (MHAQ), self-efficacy scales, and visual analogue scales (VAS) for pain and fatigue. We also compared levels of fibromyalgia (FM)-like symptoms (headache, muscle pain, numbness, and concentration problems). Scores were compared by a multivariate analysis of covariance (ANCOVA), adjusted for age, number of comorbidities, and years of education. Sime's procedure was used to adjust for multiple testing. RESULTS: RA patients had significantly lower levels of physical functioning compared to HOA patients, whereas pain measured on the Arthritis Impact Measurement Scale 2 (AIMS2) was significantly worse in HOA as compared with RA. The HOA patients also had worse scores for FM-like symptoms. SF-6D utility scores in HOA and RA were similar (0.63 and 0.64, respectively). CONCLUSIONS: The overall impact of the disease on HRQoL was similar between RA and HOA patients, based on the SF-6D scores. Physical function was worse in RA patients, but HOA patients reported worse scores in pain measures and FM-like symptoms.
21044435 Efficacy of methotrexate in comparison to biologics in rheumatoid arthritis. 2010 Sep This paper reviews trials comparing the efficacy of MTX and biologic agents. So far, the clinical evaluations of 9 biologics have been published. Three TNF inhibitors - etanercept, adalimumab, golimumab - and the IL 6 receptor inhibitor tocilizumab have been investigated in MTX naïve patients using a parallel design. The trials had 3 treatment arms: monotherapies of MTX and of the biologic compound, and the combination of both. The other biologics - infliximab, certolizumab pegol, anakinra, rituximab, and abatacept - were investigated in patients who experienced inadequate response to MTX, and were treated with MTX + biologic agent versus MTX + placebo. That design does not provide a real comparison between MTX and the biologics but may indirectly give an indication of the relative efficacy of the different biologic agents. In all trials providing a head to head comparison, MTX and biologics were similarly effective as measured by ACR and EULAR response criteria including clinical remission. In general, improvement started earlier with biologic treatment than with MTX therapy. Inhibition of radiological progression was stronger with biologics probably since TNF inhibitors, in addition to their anti-inflammatory effect, directly reduce osteoclast activity. The efficacy of biologics was significantly potentiated when they were combined with MTX. Based on the trial results the efficacy of MTX may be underestimated: the initial dose of MTX was too low and was increased only gradually. The trial design with ITT analysis and LOCF may have been disadvantageous for MTX since more patients treated with MTX withdrew and thereby had less time under treatment. Folic acid supplementation may have reduced the efficacy of MTX by interfering with its mechanism of action. Nonetheless, all trials confirmed a surprisingly good performance of MTX in comparison with biologics.
20933009 Grape seed proanthocyanidin extract (GSPE) differentially regulates Foxp3(+) regulatory an 2011 Mar 30 Grape seed proanthocyanidin extract (GSPE), which is the antioxidant derived from grape seeds, has been reported to possess a variety of potent properties. We have previously shown that GSPE attenuates collagen-induced arthritis. However the mechanism by which GSPE regulates the immune response remains unclear, although it may involve effects on the regulation of pathogenic T cells in autoimmune arthritis. To clarify this issue, we have assessed the effects of GSPE on differential regulation of Th17 and regulatory T (Treg) cells subsets in vitro in mouse and human CD4(+) T cells. We observed that GSPE decreased the frequency of IL-17(+)CD4(+)Th17 cells and increased induction of CD4(+)CD25(+)forkhead box protein 3 (Foxp3)(+) Treg cells. In vivo, GSPE effectively attenuated clinical symptoms of established collagen-induced arthritis in mice with concomitant suppression of IL-17 production and enhancement of Foxp3 expression (type II collagen-reactive Treg cells) in CD4(+) T cells of joints and splenocytes. The presence of GSPE decreased the levels of IL-21, IL-22, IL-26 and IL-17 production by human CD4(+) T cells in a STAT3-dependent manner. In contrast, GSPE induces Foxp3(+) Treg cells in humans. Our results suggest that GSPE possesses a reciprocal control over IL-17 and Foxp3. By potently regulating inflammatory T cell differentiation, GSPE may serve as a possible novel therapeutic agent for inflammatory and autoimmune diseases, including rheumatoid arthritis.
20805296 Genetic variants within the MAP kinase signalling network and anti-TNF treatment response 2011 Jan BACKGROUND: Rheumatoid arthritis (RA) does not always respond to available treatments, including tumour necrosis factor (TNF) antagonists. A study was undertaken to investigate whether genetic variation within genes, encoding proteins in the p38 signalling network, contributes to the variable response to TNF antagonists. METHODS: 1102 UK Caucasian patients with RA receiving anti-TNF therapy (infliximab, adalimumab and etanercept) were genotyped for 38 pairwise-tagging single nucleotide polymorphisms (SNPs) spanning 12 candidate genes from the p38 network. Regression analyses were performed to test association between genotype and treatment response at 6 months using both absolute change in DAS28 (Disease Activity Score across 28 joints) and European League Against Rheumatism (EULAR) improvement criteria. Stratified analyses were performed to investigate association with individual therapies. RESULTS: Seven SNPs, in five genes, were associated with improvement in DAS28 at 6 months at a nominal 0.1 significance level, jointly explaining 3% of variance in outcome in a model adjusting for other predictors. These encoded proteins both upstream (MKK6) and downstream (MAPKAPK2, MSK1, MSK2) of p38, and MAPK14, the p38-α isoform of p38 MAPK. One SNP (rs2716191 in MAP2K6) was associated with EULAR response at the 0.1 level. SNPs generally showed greater correlation with response to infliximab and adalimumab, but not to etanercept. CONCLUSIONS: More SNPs than would be expected by chance, mapping to the p38 signalling network, showed association with the anti-TNF response as a whole, and particularly with the response to infliximab and adalimumab. Validation of these findings in independent cohorts is warranted.
20081712 EROMIA in inflammatory arthritis: the next step in standard practice. 2010 Jan 14 Patient reported outcome measures (PROMs) have been increasingly recognized as important tools in rheumatoid arthritis. PROMs add up to a composite score that directly reflects changes in outcomes of immediate importance to patients on a daily basis, such as pain, sleep, fatigue, functional impairment and quality of life. Prospective collection of the patients' information in databases has been attempted, mainly in research studies. This work was carried out to assess the possibility of systematically collecting and aggregating a focused set of clinical data in the standard clinical practice, directly and comfortably from the point of care and on an ongoing basis, using EROMIA software. Recording the patients' data electronically has significantly (P<0.01) saved time in comparison with written paper format. It also significantly (P<0.001) saved time in retrieving patients' recorded data. In addition to the traditional disease outcome measures, disease comorbidities such as falls and cardiovascular risks could be recorded. Recording tender and swollen joints individually was made possible. EROMIA offered a hospital-based integrated monitoring database that echoes daily clinical practice. It does not require advanced computer knowledge.
19473573 Differential association of the N-propeptide of collagen IIA (PIIANP) and collagen II C-te 2009 Mar OBJECTIVES: To determine the N-terminal propeptide of collagen IIA (PIIANP) in early and established rheumatoid arthritis (RA) and to study the association with collagen II degradation assessed by its C-telopeptide (CTX-II), x-ray status and disease activity measures. METHODS: Two cohorts of RA patients were included: A) a one-year prospective cohort including 45 patients with early, untreated RA and B) a cross-sectional study comprising 50 RA patients with advanced disease. Blood donors and healthy volunteers served as controls. PIIANP in serum and urine CTX-II were measured by ELISA. RESULTS: PIIANP did not differ from control levels at any time in patients with early RA (p=0.16 and p=0.89), but at one-year follow-up, PIIANP was decreased compared with baseline (p=0.046). In patients with longstanding RA, PIIANP was lower than in controls (p=0.002) and RA patients with a 12-month disease (p=0.01). PIIANP was unrelated to joint counts and CRP in both cohorts, but baseline PIIANP was lower among x-ray progressors than in non-progressors (p=0.04). CTX-II was persistently increased in both cohorts (p<0.001 and p<0.001). CTX-II was positively associated with joint counts and CRP but not with x-ray progression (p=0.84). There was no correlation between PIIANP and CTX-II. CONCLUSION: Declining PIIANP with increasing RA duration and persistently increased CTX-II indicate that cartilage anabolic and degradative pathways are unbalanced from clinical RA onset. Furthermore, that collagen II depletion in RA is both mediated by anti-anabolic effects unassociated with synovitis (decreased PIIANP) and by excess collagen II degradation linked to synovitis (increased CTX-II).