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ID PMID Title PublicationDate abstract
11120612 Genetic diversity in Proteus mirabilis isolates found in the urinary tract of rheumatoid a 2000 Nov OBJECTIVE: Elevated levels of anti-Proteus antibodies but not antibodies to E. coli have been reported in patients with rheumatoid arthritis (RA). The suggestion has been made that P. mirabilis may have a role in the aetiopathogenesis of rheumatoid arthritis. The aim of this study was to determine whether there are differences at the genetic level inisolates of P. mirabilis obtained from controls and RA patients. METHODS: A blind study was performed whereby P. mirabilis isolates obtained from urinary cultures of RA patients and controls were analysed using RAPD PCR. Isolates were then grouped on the basis of their DNA band profile after agarose gel electrophoresis, thereby allowing the composition of the Proteus population in the urinary tract to be analysed at the genetic level. RESULTS: Fourteen different DNA band profiles were obtained from the 93 isolates tested: 70% of these isolates fell into only five of the 14 groups and approximately 25% of all isolates fell into one group. No differences were observed in the frequency of isolates from either control or RA subjects. CONCLUSIONS: There is genetic diversity in P. mirabilis populations found in the urinary tract, but there are no differences in the frequency of these bacteria between RA patients and controls.
11484878 Induction of a novel gelatinolytic activity in synovial tissue of patients with rheumatoid 2000 Gelatinolytic activity induced by longtime incubation at 37 degrees C was found in extracts of rheumatoid synovial tissues. The enzyme activity was assessed by gelatin zymography and 3H-gelatin degradation assay. The observed enzyme had different characteristics from matrix metalloproteinases; it did not require metal ions for activity. However, metallocheltors blocked activation and addition of some metal ions restored the activation. The molecular size of the enzyme was changed time-dependently. The approximate molecular weight of the first enzyme produced by incubation was 65 kDa and it was converted to a broad size molecule with a molecular weight of 50 kDa after further incubation. Substrate specificity was detected for denatured collagen types I, II, III and IV.
9973155 A new antibody in rheumatoid arthritis targeting glycated IgG: IgM anti-IgG-AGE. 1998 Dec Hyperglycaemia and/or oxidative stress can cause IgG to be modified by advanced glycation end products (AGE). Three patients with aggressive rheumatoid arthritis (RA) and vasculitis are described who have high titres of IgM antibodies against AGE-modified IgG (IgM anti-IgG-AGE). Diabetics and randomly selected patients with rheumatic diseases, including 50 additional RA patients, were tested for IgM and IgA anti-IgG-AGE by ELISA. AGE-modified proteins were detected using the nitroblue tetrazolium (NBT) colorimetric method. The presence of Nepsilon (carboxymethyl) lysine, an AGE modification, was detected on IgG-AGE by immunoblotting. A total of 20/41 (49%) rheumatoid factor (RF)-positive RA patients tested had IgM anti-IgG-AGE antibodies, 4/12 (33%) RF-positive systemic lupus erythematosus (SLE) patients, 3/5 RF-positive patients with primary Sjogren's syndrome (SS), and 3/5 RF-positive diabetics. All patients with RF-negative RA, SLE, SS, osteoarthritis (24), spondyloarthritis (15), adult-onset Still's disease (8), diabetes (25) and healthy controls (20) were anti-IgG-AGE negative. RF and IgM anti-IgG-AGE appeared to be a linked response. The IgM anti-IgG-AGE, along with IgG-AGE, may contribute to the pathogenesis of RA.
11196512 Interleukin 16 expression in relation to disease activity in rheumatoid arthritis. 2001 Jan OBJECTIVE: Rheumatoid arthritis (RA) is a chronic inflammatory disease of unknown etiology characterized by an infiltration of CD4+ T lymphocytes within the rheumatoid synovium. Cytokines have been shown to play a modulatory role in the pathogenesis of RA. We analyzed the expression of a T cell derived cytokine. interleukin 16 (IL-16), in relation to disease activity to characterize its biologic function in RA. METHODS: Secreted IL-16 was measured by enzyme immunoassay in sera and synovial fluids (SF) from 25 patients with RA in comparison to 20 control samples from patients with osteoarthritis (OA). IL-16 expression in peripheral blood mononuclear cells (PBMC) was characterized by flow cytometric analysis after intracellular cytokine staining for IL-16. In synovial tissue specimens, IL-16 mRNA expression was analyzed by real-time quantitative reverse transcriptase polymerase chain reaction (RT-PCR). In parallel, expression of IL-16 was localized in synovial tissues by in situ hybridization and immunohistochemistry. Results were analyzed in relation to disease activity. RESULTS: IL-16 was detected at significantly higher levels in sera and SF of patients with RA in comparison to OA (p < 0.001). Flow cytometry of PBMC showed that a great proportion of both CD4+ and CD8+ T cells constitutively expressed the IL-16 protein. In synovial tissues, IL-16 mRNA levels were significantly elevated in comparison to OA controls (p < 0.001). In situ hybridization for IL-16 producing cells revealed a predominant accumulation of IL- 16 positive cells within the inflammatory infiltrates. A significant correlation between IL- 16 expression and local inflammatory activity could not be established (r = 0.27, p = 0.19) by microscopic analysis of the synovial cell infiltrate. In addition, no significant association was observed between serum, SF, and synovial tissue expression of IL-16 and clinical disease activity in RA. CONCLUSION: These data suggest IL-16 might play a role in the pathogenesis of chronic inflammation in RA. The lack of significant correlation between IL-16 expression, clinical disease activity, and local inflammatory activity suggests a regulatory rather than a proinflammatory function for IL-16 in the pathogenesis of chronic synovial inflammation in RA.
9712083 A randomized, double blind, placebo controlled multicenter trial of murine anti-CD4 monocl 1998 Aug OBJECTIVE: To assess safety and efficacy of a murine anti-CD4 monoclonal antibody (Mab) in a population of patients with rheumatoid arthritis (RA) compared to treatment with placebo. METHODS: Fifty-eight patients with defined RA were included in this placebo controlled, randomized, double blind, multicenter study. Of the 48 women and 10 men (mean age 54.5 years), 25 were functional class II and 31 were class III, with 9 years' disease duration; the mean of previous disease modifying antirheumatic drugs was 4; 49 were taking steroids (mean dosage 11 mg/day of prednisone). Eighty percent were rheumatoid factor positive. All were in an active state of the disease with: pain > 4 (mean at inclusion 6.6), tender joints > 4 (mean 12), swollen joint count > 3 (mean 9), morning stiffness > 45 min (mean 185), erythrocyte sedimentation rate > 30 mm (mean 59) or C-reactive protein (CRP) > 30 mg/l (mean 63). Treatment was randomized between murine anti-CD4 Mab (B-F5, Diaclone, 20 mg/day) or placebo intravenously for 10 consecutive days. Efficacy was assessed with a composite index (Paulus), with evaluation of number of patients with 20 or 50% improvement in each group. Changes in measures of single clinical or biological variables were also evaluated. RESULTS: The 2 groups were comparable at inclusion. Treatment was well tolerated. Mild side effects (chills, fever, rash) were seen in both groups. Percentage of patients with global 20 or 50% response did not differ between placebo and Mab groups at Day 10 or at Day 30. Evaluation of single variables showed reduced CRP, swollen joint count, and Ritchie index in some B-F5 patients at Day 10, although in the B-F5 group as a whole only CRP was significant. CONCLUSION: No significant improvement in RA after murine anti-CD4 Mab was observed.
10689949 [Use of glucocorticoids in rheumatoid arthritis]. 2000 Feb 7 OBJECTIVES: To determine whether short-term (i.e. as recorded within the first month of therapy), oral low-dose corticosteroids (corresponding to a maximum of 15 mg prednisolone daily) is superior to placebo and nonsteroidal, antiinflammatory drugs in patients with rheumatoid arthritis. SEARCH STRATEGY: Medline Silverplatter, The Cochrane Controlled Trials Register, reference lists and a personal archive. SELECTION CRITERIA: All randomised studies comparing an oral corticosteroid (not exceeding an equivalent of 15 mg prednisolone daily) with placebo or a nonsteroidal, antiinflammatory drug were eligible if they reported clinical outcomes within one month after start of therapy. DATA COLLECTION AND ANALYSIS: Decisions on which trials to include were made independently by two observers based on the methods sections of the trials only. Standardised effect measures were used for the statistical analyses; the random effects model was used if p < 0.10 for the test of heterogeneity. MAIN RESULTS: Ten studies, involving 320 patients, were included in the meta-analysis. Prednisolone had a marked effect over placebo on joint tenderness (standardised effect size 1.31, 95% confidence interval 0.78 to 1.83), pain (standardised effect size 1.75, 0.87 to 2.64) and grip strength (standardised effect size 0.41, 0.13 to 0.69). Measured in the original units, the differences were 12 tender joints (6 to 18) and 22 mmHg (5 to 40) for grip strength. Prednisolone also had a greater effect than nonsteroidal, antiinflammatory drugs on joint tenderness (standardised effect size 0.63, 0.11 to 1.16) and pain (standardised effect size 1.25, 0.26 to 2.24), whereas the difference in grip strength was not significant (standardised effect size 0.31, -0.02 to 0.64). Measured in the original units, the differences were 9 tender joints (5 to 12) and 12 mmHg (-6 to 31). The risk of adverse effects, also during moderate- and long-term use, seemed acceptable. CONCLUSIONS: Prednisolone in low doses (not exceeding 15 mg daily) may be used intermittently in patients with rheumatoid arthritis, particularly if the disease cannot be controlled by other means. Since prednisolone is highly effective, short-term placebo controlled trials studying the clinical effect of low-dose prednisolone or other oral corticosteroids are no longer necessary.
10371284 Positive association of the HLA DMB1*0101-0101 genotype with rheumatoid arthritis. 1999 May OBJECTIVE: HLA DM is a non-classical major histocompatibility complex (MHC) class II molecule that has been shown to facilitate peptide loading with classical class II molecules. METHODS: In this study, we analysed the polymorphism in exon 3 of HLA DMA and DMB genes by a polymerase chain reaction-sequence-specific oligonucleotide probe method in 163 rheumatoid arthritis (RA) patients and 146 ethnically matched controls. The HLA-DRB1 genotype was also analysed by a reverse-dot blot method. RESULTS: Our results show in RA patients a significant increase in the HLA DMB*0101 allele frequency (83% vs 72.3% of the controls, P < 1.6 x 10(-3), significance at P < 0.0125) and in the HLA DMB*0101-0101 homozygote genotype frequency [70.8% vs 50% of the controls, P < 4.2 x 10(-4), significance at P < 0.00625, odds ratio (OR) = 2.4, 95% confidence interval (CI): 1.43-4]. The increase in DMB*0101 allele and homozygote genotype frequencies was independent of a linkage disequilibrium between DMB and DRB1 alleles. The analysis of non-random associations between the HLA-DM and DRB1 alleles only revealed a significant association in controls between DMB*0104 and DRB1*07 alleles (delta = 0.01, P < 7 x 10(-4), significance at P < 9.6 x 10(-4)). On the other hand, the DMB*0101-0102 genotype frequency was increased in DRB1*0401-negative RA patients as compared to controls (11% vs 2%, P < 0.011, significance at P < 0.015, OR = 6.2, 95% CI: 1.2-30). CONCLUSION: Our data suggest that HLA-DM alleles could play a role in the genetic susceptibility to RA.
9742822 [A case report of aortic regurgitation associated with rheumatic arthritis]. 1998 Aug We report a rare case of aortic regurgitation (AR) associated with rheumatic arthritis (RA). A 61-year-old female was admitted to our hospital with severe heart failure due to AR. She had a 8-year history of RA and had been treated with steroid therapy. Trans-esophageal echocardiography showed thickness and shortening of non coronary cusp (NCC) of aortic valve. After treated for heart failure, aortic valve replacement with SJM-HP 17 mm was done. At operation, right and left coronary cusps were almost normal, but NCC was thickened and shortened. The valve of NCC histology showed granuloma. She recovered uneventfully. Two cases of cardiac valvular disease, associated with granuloma of RA, were reported in Japan. We discussed these cases in this paper.
10529245 Mechanism of hypochlorite-mediated inactivation of proteinase inhibition by alpha 2-macrog 1999 Oct 19 The proteinase-proteinase inhibitor balance plays an important role in mediating inflammation-associated tissue destruction. alpha 2-Macroglobulin (alpha 2M) is a high-affinity, broad-spectrum proteinase inhibitor found abundantly in plasma and interstitial fluids. Increased levels of alpha 2M and proteinase-alpha 2M complexes can be demonstrated in patients with sepsis, emphysema, peridontitis, rheumatoid arthritis, and other inflammatory diseases. Despite these increased levels, proteolysis remains a significant problem. We hypothesized that a mechanism for inactivating alpha 2M-mediated proteinase inhibition must exist and recently demonstrated that alpha 2M isolated from human rheumatoid arthritis synovial fluid is oxidized and has decreased functional activity. The oxidant responsible for alpha 2M inactivation and the mechanism of such destruction were not studied. We now report that while hypochlorite and hydroxyl radical both modify amino acid residues on alpha 2M, only hypochlorite can abolish the ability of alpha 2M to inhibit proteinases. Hydrogen peroxide, on the other hand, has no effect on alpha 2M structure or function. Protein unfolding with increased susceptibility to proteolytic cleavage appears to be involved in alpha 2M inactivation by oxidation. The in vivo relevance of this mechanism is supported by the presence of multiple cleavage fragments of alpha 2M in synovial fluid from patients with rheumatoid arthritis, where significant tissue destruction occurs, but not in patients with osteoarthritis. These results provide strong evidence that hypochlorite oxidation contributes to enhanced tissue destruction during inflammation by inactivating alpha 2M.
11929590 Combination of HLA-A and HLA class II alleles controls the susceptibility to rheumatoid ar 2001 Dec Two hundred and four unrelated Japanese patients with rheumatoid arthritis (RA) were typed for HLA by serological typing and DNA typing. The serological typing revealed that frequencies of HLA-A11, DR4, DR53 and DQ4 were increased and those of DR8 and DQ1 were decreased in the patients. The DNA typing has precisely defined the disease-associated HLA class II alleles; DRBl*0405, DQAl*03 and DQBl*0401 showed positive associations, while negative associations were found with DRBl*0803, DQAl*0103 and DQBl*0601. The risk for RA was found to be closely associated with particular amino acid sequences of DR-beta chain, including glycine residue at the 86th position in addition to those between 70 and 74, which are known to confer binding specificity and affinity to antigenic peptides. The observation that the frequency of HLA-A11 was increased in the DRBl*0405-positive patients suggested the interaction of these two alleles in the susceptibility to RA. On the other hand, the frequency of DPB1*0201 was increased in the DRBl*0405-negative patients and the frequency of HLA-A2 was increased in the DPBl*0201-positive patients, especially in the younger onset group. These findings suggested that the combination of HLA-A2 and DPBl*0201 may confer the susceptibility in the DRBl*0405-negative patients. Our results suggested the possibility that the susceptibility to RA is controlled by the interaction of HLA-A and DRBl genes or by that of HLA-A and DPBl genes in different patient subgroups.
11502614 Effect of patient education on adherence to drug treatment for rheumatoid arthritis: a ran 2001 Sep OBJECTIVE: To determine whether a patient education programme (PE) would improve rates of adherence to a slow acting antirheumatic drug and to assess any subsequent effect on patient outcome. METHODS: A randomly controlled study comprising 100 patients with rheumatoid arthritis (49 control CG; 51 experimental EG) requiring D-penicillamine (DPA). The same practitioner saw patients on seven occasions, for the same length of time. The EG received 7 x 30 minute one to one sessions of PE, while the CG received standard management. The primary measure of adherence was a pharmacological marker (phenobarbitone) encapsulated with the DPA assayed at monthly intervals for six months. Plasma viscosity (PV), C reactive protein, articular index, morning stiffness, and pain score were used to assess outcome. RESULTS: 454 blood samples were collected and assayed and the pharmacological marker showed the EG to be significantly more adherent on more occasions than the CG (p<0.05). Patterns of adherence over time showed that at 12 weeks 86% (38/44) of those in the EG compared with 64% (29/45) of the CG remained adherent (p=0.01). These trends continued and by the end of the study 85% (29/34) of the EG compared with 55% (23/42) of the CG were taking their DPA as prescribed. Fifteen patients (12 from the EG) experienced side effects requiring study withdrawal and 14 patients requested study withdrawal (two from the EG). On study entry patients in the CG had significantly higher levels of PV than the EG and this remained so throughout the research. However, on completion, the health status of patients in both groups had improved significantly (p<0.01). CONCLUSIONS: PE significantly increased adherence to DPA and its effects persisted over a period of six months. No additional clinical benefit was detected in the EG in comparison with the CG.
11350844 Comparative study of intramuscular gold and methotrexate in a rheumatoid arthritis populat 2001 Jun OBJECTIVE: To compare the risk-benefit ratio of intramuscular gold (gold sodium thiomalate (GST)) and methotrexate (MTX) in a population with rheumatoid arthritis (RA) from a deprived area. METHODS: Patients with active RA were randomly assigned to open treatment with GST or MTX. Clinical and laboratory assessment was performed at 0, 12, 24, and 48 weeks. Results were analysed on an intention to treat basis. RESULTS: 141 patients were recruited-72 were randomly allocated to GST and 69 to MTX. There were no statistically significant differences found in either the clinical or demographic variables at baseline. At 48 weeks 31 (43%) patients continued to receive GST and 43 (62%) MTX. The median MTX dose achieved was 10 mg. Gold caused significantly more withdrawals for toxicity (43% GST v 19% MTX, p=0.0026, log rank test). Both groups experienced a significant improvement in erythrocyte sedimentation rate, C reactive protein, Ritchie Articular Index, and pain score by 24 weeks (p<0.001, Friedman test). Although a trend towards an improved Health Assessment Questionnaire (HAQ) score and global wellbeing was seen in both groups, this did not reach statistical significance. No differences in efficacy were found when the two groups were compared (Mann-Whitney). CONCLUSION: GST and low dose MTX showed equivalent efficacy, but toxicity was more common in patients treated with GST. GST, although more toxic, remains a useful alternative for patients in whom MTX is contraindicated.
9779840 Cysteine proteinase cathepsin K mRNA is expressed in synovium of patients with rheumatoid 1998 Oct OBJECTIVE: Cysteine proteinases B and L have been shown to be involved in matrix degradation of joints in patients with rheumatoid arthritis (RA). Since the cysteine proteinase cathepsin K is assumed to play a pivotal role in osteoclast mediated bone resorption, we investigated the expression of cathepsin K in RA joints. METHODS: We studied 10 RA and 4 normal synovial specimens and 5 articular heads with RA lesions by in situ hybridization, applying specific riboprobes for cathepsin K, human collagen type I, and cathepsin B. Antibodies against monocyte/macrophage associated CD68 antigen were applied in immunohistochemistry. Reverse transcription-polymerase chain reaction (RT-PCR) and ribonuclease protection assay (RPA) were performed on 4 RA, 1 normal, and 1 immortalized normal fibroblast cultures. RESULTS: Cathepsin K mRNA expression was upregulated in RA synovium compared to normal synovium. Cathepsin K mRNA was expressed mainly by synovial fibroblasts. These data were confirmed by RT-PCR and RPA. In RA articular heads, cathepsin K mRNA was detected at sites where synovium attached and invaded underlying bone. The cells at these sites represented collagen type I and cathepsin B mRNA expressing fibroblasts as well as CD68+ macrophages and giant cells. In addition, a distinct expression of cathepsin K mRNA was also detected around lymphocytic infiltrates in RA synovium. CONCLUSION: The data indicate that cathepsin K is not only expressed by osteoclasts but also by synovial fibroblasts, and suggest that cathepsin K contributes to bone destruction mediated by RA synovial cells. The expression of cathepsin K around lymphocytic infiltrates suggests further to facilitate the movement of mononuclear cells through the perivascular interstitial matrix and thereby contribute to interstitial matrix turnover.
9068281 Study of eight cases of cancer in 426 rheumatoid arthritis patients treated with methotrex 1997 Feb OBJECTIVE: To report cancer cases in 426 rheumatoid arthritis patients treated with methotrexate, and determine whether there was an increased incidence of cancer compared with patients never treated with methotrexate (rheumatoid controls) and to the whole regional population. METHODS: The duration of methotrexate treatment was 37.4 (SD 27.9) months. This population was compared with 420 rheumatoid arthritis controls and with a regional population of 812,344 people. Life table analysis was performed to compare the cancer incidence in the two rheumatoid populations. Adjustment for potentially confounding factors was done. The indirect standardisation methods was used to compare each rheumatoid population with the regional population. RESULTS: Eight cases of cancer (1.88%; 4.04 cases/1000 person years) were diagnosed in the methotrexate population v six (1.43%; 58.8 cases/1000 person years) in the rheumatoid controls. The life table method showed a higher incidence of cancer in the rheumatoid controls (P = 0.0001). In a multivariate analysis (Cox model), the only significant factor explaining this difference in the cancer incidence was age (P = 0.02). In the regional population there were 6418 new cases of cancer (0.79%; 2.85 cases/1000 person years). By the indirect standardisation method, the ratio of observed cases to expected cases of cancer in each of the rheumatoid populations was not significantly different from 1. CONCLUSIONS: In these eight cases, methotrexate was not found to be responsible for generating cancers. However, because of data regarding lymphomas and methotrexate, and because of the short follow up, especially in the control group, longer prospective studies are warranted.
11327276 Minimal clinically important difference in plain films in RA: group discussions, conclusio 2001 Apr Analysis of progression of structural damage on an individual patient level in randomized controlled trials provides extra information in addition to the analysis on a group level. A cutoff level is required to define which patients show progression and which patients do not. The objective of the mimimal clinically important difference (MCID) module for plain films was to elaborate the various concepts to determine a MCID for plain films, and if possible, to define a MCID for specific scoring methods. The module comprised preconference reading material, a plenary session, small group discussions, and a plenary report of the group sessions, combined with interactive voting. The following conclusions and recommendations were made: the smallest detectable difference (SDD) beyond measurement error is a good starting point to define MCID; SDD is study-specific; SDD should be reported for all radiographic endpoints used in a trial as a quality control; the expert panel approach is a reasonable method to define MCID, but defined in this way MCID may be smaller than current SDD; more research is needed to validate expert panel based MCID in different datasets and with different experts; a predictive, data driven MCID is the ultimate goal, but is not yet available; the SDD can be used as a proxy for MCID until a data driven MCID is available; analysis at the group level (comparison of means or medians) should remain primary in studies that include progression of joint damage as outcome measure; the proportion of patients showing more progression than the SDD is a secondary outcome measure.
9808398 Three dimensional CT evaluation of occipito-atlanto-axial dislocation in rheumatoid arthri 1998 Involvement of the upper cervical spine, with possible instability and dislocation of the atlanto-axial-cervico-occipital joints in patients with rheumatoid arthritis (RA), is routinely monitored with conventional radiographs. As disease progresses severe interpretation problems occur, especially when looking for cranial migration of the odontoid process. The aim of the present study was to evaluate whether three dimensional CT examination should be considered for such monitoring. After clinical and biochemical examination of 20 consecutive patients, diagnostic information about cranial migration of the odontoid process was obtained by conventional radiograms and by three dimensional CT examination. When using conventional radiographs the odontoid process and the its relation to the skull base could be outlined in 8 of the 20 patients. whereas all bony structures could be well demonstrated on the CT examination and the degree of cranial migration into the foramen magnum could be quantified. Three dimensional CT should be considered as a reliable examination for monitoring RA patients with involvement of the upper cervical spine and a possible cranial migration of the odontoid process.
11679601 Kudo total elbow arthroplasty in patients with rheumatoid arthritis: a long-term follow-up 2001 Oct BACKGROUND: Improvements in the design of total elbow prostheses over the last two decades have led to better and more consistent results. The type-3 Kudo total elbow prosthesis was developed in 1980. The long-term results of use of this implant have not been reported. Because it is an unlinked prosthesis, it is not known whether preservation of the anterior oblique component of the ulnar collateral ligament at the time of implantation is important. METHODS: A type-3 Kudo total elbow arthroplasty with cement was performed in forty-seven patients (fifty elbows) with rheumatoid arthritis. Revision rates, clinical symptoms, postoperative complications, and radiographic changes were assessed eleven to sixteen years (mean, thirteen years) postoperatively. RESULTS: The overall survival rate of the prosthesis was 90% at sixteen years. The mean Mayo elbow performance scores were all poor (mean overall score, 43 points) initially. The overall score was substantially improved at both the intermediate follow-up examination (four to six years after the operation) and the late follow-up examination (eleven to sixteen years after the operation), to 81 and 77 points, respectively. The overall rate of radiolucency about the humeral component was 45% at the intermediate follow-up examination and 100% at the long-term follow-up examination. The rate of radiolucency about the ulnar component at the intermediate and late follow-up examinations was 4.3% and 8.9%, respectively. No great differences in results were found with preservation of the anterior oblique component of the ulnar collateral ligament. CONCLUSIONS: This long-term follow-up study showed acceptable results of the type-3 Kudo total elbow arthroplasty in patients with rheumatoid arthritis. Preservation of the ulnar collateral ligament does not seem to be necessary when performing this procedure.
10909593 [Chemical synovectomy in arthritis by intra-articular injection of osmic acid]. 1998 Apr 1 18 patients suffering from persistent synovitis despite medical therapy were treated with an intra-articular injection of osmic acid. After 1 year of follow-up, 68% had good results and there were no complications nor detectable radiographic evidence of disease progression. Because osmic acid is almost as effective as surgical synovectomy and is cheap and easy to administer, it can be recommended as the first choice for treatment of corticosteroid-resistant arthritis in the early stages of the disease.
9352601 Xenobiotic immunosuppressive agents: therapeutic effects in animal models of autoimmune di 1997 An unprecedented arsenal of new xenobiotic immunosuppressive agents has been developed recently. Most of the new immunosuppressants have been tested primarily in the treatment of allograft rejection in experimental models of transplantation, and some of the new drugs have already proven their safety and efficiency in extensive clinical trials on transplant patients. Another field for their potential application is the treatment of autoimmune diseases. This review will give an overview of the therapeutic potential of the new xenobiotic drugs in different animal models of rheumatoid arthritis, systemic lupus erythematosus, myasthenia gravis, multiple sclerosis, diabetes mellitus, thyroiditis and uveoretinitis. The new xenobiotics are either inhibitors of the de novo synthesis of nucleotides, for example mycophenolate mofetil, mizoribine, leflunomide, and brequinar, or are immunophilin-binding agents (cyclosporin, FK506 and rapamycin) that inhibit signal transduction and cell cycle progression in lymphocytes. A different mode of action is likely to account for the immunosuppressive effects of deoxyspergualin, which may interfere with intracellular chaperoning by the heat shock protein HSP70 and the activation of transcription factor NF-kappa B.
11352263 Complement activation in patients with rheumatoid arthritis mediated in part by C-reactive 2001 May OBJECTIVE: Complement activation in patients with rheumatoid arthritis (RA) is considered to be triggered by immune complexes. Recently, it was shown that C-reactive protein (CRP) can activate the complement system in vivo. We therefore hypothesized that part of the complement activation in RA is due to CRP. The aim of this study was to investigate CRP-mediated complement activation in RA, and to assess its correlation with disease activity. METHODS: Complexes between CRP and the activated complement components C3d (C3d-CRP) and C4d (C4d-CRP), which reflect CRP-mediated complement activation, as well as the overall levels of activated C3 and C4 were measured in the plasma of 107 patients with active RA and 177 patients with inactive RA. Inactive RA was defined according to the American College of Rheumatology criteria for clinical remission. Disease activity was assessed by the modified Disease Activity Score (DAS28). RESULTS: Plasma levels of C3d-CRP and C4d-CRP were increased in the majority of the patients, and were significantly higher in patients with active disease versus those with inactive RA (P < 0.001). In patients with active RA, the plasma concentrations of C3d-CRP and C4d-CRP correlated significantly with the DAS28 (Spearman's rho 0.61 and 0.55, respectively; P < 0.001), whereas these correlations were less pronounced in patients with inactive RA (Spearman's rho 0.28 [P < 0.001] and 0.25 [P = 0.001], respectively). Levels of activated C3 and C4 were also increased in the majority of the patients, particularly in patients with active RA. CONCLUSION: Part of the activation of complement in RA is mediated by CRP and is correlated with disease activity. We suggest that this activation is involved in the pathogenesis of RA.