British journal of rheumatology最新文献

{"title":"Surface-associated protein from Staphylococcus aureus stimulates osteoclastogenesis: possible role in S. aureus-induced bone pathology.","authors":"S Meghji,&nbsp;S J Crean,&nbsp;P A Hill,&nbsp;M Sheikh,&nbsp;S P Nair,&nbsp;K Heron,&nbsp;B Henderson,&nbsp;E B Mawer,&nbsp;M Harris","doi":"10.1093/rheumatology/37.10.1095","DOIUrl":"https://doi.org/10.1093/rheumatology/37.10.1095","url":null,"abstract":"<p><strong>Objective: </strong>Staphylococcus aureus is the cause of bone destruction in osteomyelitis, bacterial arthritis and orthopaedic implant failure. We have previously shown that gentle saline extraction of S. aureus has revealed the presence of an extremely potent stimulator of osteoclast activation in both the murine calvarial bone resorption assay and the isolated chick osteoclast resorption assay. In order to investigate the mechanism of action of this surface-associated material (SAM), we have investigated its capacity to recruit osteoclasts.</p><p><strong>Methods: </strong>The murine bone marrow osteoclast recruitment assay was used. The ability of the recruited cells to resorb dentine slices was also investigated. Results. The SAM from S. aureus dose dependently stimulated tartrate-resistant acid phosphatase (TRAP)-positive osteoclast formation and pit formation on dentine slices. Neutralization of the cytokines tumour necrosis factor alpha and interleukin (IL)-6 totally inhibited, but antagonism of IL-1 only partially blocked, the stimulated maturation of osteoclast-like cells.</p><p><strong>Conclusion: </strong>These findings suggest that bone destruction associated with local infection by S. aureus is due to the stimulation of osteoclast formation induced by the action of the easily solubilized SAM, and could explain the large numbers of osteoclasts found in infarcted bone in osteomyelitis.</p>","PeriodicalId":9307,"journal":{"name":"British journal of rheumatology","volume":"37 10","pages":"1095-101"},"PeriodicalIF":0.0,"publicationDate":"1998-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1093/rheumatology/37.10.1095","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20736973","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-beta2-glycoprotein I, anti-prothrombin and anticardiolipin antibodies in a longitudinal study of patients with systemic lupus erythematosus and the antiphospholipid syndrome.","authors":"M. Inanç, S. Donohoe, C. Ravirajan, E. Radway-Bright, I. Mackie, S. Machin, D. Isenberg","doi":"10.1093/RHEUMATOLOGY/37.10.1089","DOIUrl":"https://doi.org/10.1093/RHEUMATOLOGY/37.10.1089","url":null,"abstract":"OBJECTIVE\u0000To determine anti-beta2 glycoprotein-I (anti-beta2GPI) and anti-prothrombin (anti-ProT) antibody levels, and the IgG subclass distribution of anti-beta2GPI antibodies, in serial samples from patients with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS) having initial or recurrent thrombotic/neurological (T/N) events during the study period. To investigate the correlations between these antibodies and beta2GPI antigen, anticardiolipin antibody (aCL), anti-double-stranded (ds) DNA, C3 levels and disease activity.\u0000\u0000\u0000METHODS\u0000Fifty serum samples were identified from seven patients with SLE who had had T/N events during the follow-up from a cohort under long-term follow-up. IgG anti-beta2GPI, anti-ProT, aCL, IgG subclasses of anti-beta2GPI and beta2GPI antigen levels were determined by ELISA. Corresponding disease activity [British Isles Lupus Assessment Group (BILAG)], anti-dsDNA and C3 levels were compared.\u0000\u0000\u0000RESULTS\u0000IgG anti-beta2GPI antibody levels were elevated in six of the patients before and after the T/N events with less marked fluctuations than aCL antibody levels. The predominant subclass of anti-beta2GPI antibodies was IgG2 before and after the T/N events. IgG anti-ProT antibodies were negative in all cases. There was a significant but weak correlation between anti-beta2GPI and aCL antibodies. No correlation was found between disease activity and IgG anti-beta2GPI antibody and beta2GPI antigen levels. There were fluctuations in beta2GPI antigen levels and a trend to increase after T/N events was observed in some patients.\u0000\u0000\u0000CONCLUSION\u0000Most of the patients with a T/N event during the study period had IgG anti-beta2GPI, but not IgG anti-ProT antibodies. Many IgG aCL-negative samples were found to have IgG anti-beta2GPI activity during the follow-up period. The predominant subclass of IgG anti-beta2GPI was IgG2, which may have importance in the pathogenesis of APS. beta2GPI antigen levels were found to be increased in some patients with SLE after T/N events. IgG anti-beta2GPI antibodies may be used as an adjunctive marker of future T/N events in patients with SLE and APS with aCL antibodies and lupus anticoagulant.","PeriodicalId":9307,"journal":{"name":"British journal of rheumatology","volume":"40 1","pages":"1089-94"},"PeriodicalIF":0.0,"publicationDate":"1998-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73011070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Can collagen type II sustain a methotrexate-induced therapeutic effect in patients with long-standing rheumatoid arthritis? A double-blind, randomized trial.","authors":"H J Häuselmann,&nbsp;M Caravatti,&nbsp;B Seifert,&nbsp;K Wang,&nbsp;P Bruckner,&nbsp;G Stucki,&nbsp;B A Michel","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objective: </strong>Based on the results of two recently published, randomized, double-blind and placebo-controlled studies, a possible improvement in rheumatoid arthritis disease activity after oral tolerization with triple helical collagen type II has been suggested. The goal of this study was to go one step further and ask the question whether collagen type II can sustain the therapeutic effect induced by methotrexate, the most widely accepted disease-modifying anti-rheumatic drug in patients with long-standing rheumatoid arthritis.</p><p><strong>Methods: </strong>Ninety-two patients with rheumatoid arthritis on stable therapy with methotrexate were enrolled in a 3 month double-blind, randomized and comparative study to examine the efficacy of oral triple helical collagen type II as compared to continuing methotrexate. The dose of methotrexate (or the respective placebo drug) and of concomitant corticosteroids was not changed and intra-articular corticosteroids were not allowed during the 3 months. The primary study endpoint was disease activity as measured by physician and patients.</p><p><strong>Results: </strong>While patients under ongoing therapy with methotrexate had, as expected, no change in disease activity, almost all parameters of disease activity and outcome in patients under a daily oral dose of 0.5 mg triple helical collagen type II worsened significantly (highly significant difference in swollen joints, between the two groups, P < 0.0001). No significant differences in side-effects between the two groups during the study period could be demonstrated.</p><p><strong>Conclusions: </strong>Substitution of methotrexate with daily 0.5 mg of triple helical collagen type II in patients with rheumatoid arthritis leads to a significant increase in disease activity, suggesting that oral collagen type II at the given dose is not capable of sustaining the methotrexate-induced anti-inflammatory effect in patients with long-standing rheumatoid arthritis.</p>","PeriodicalId":9307,"journal":{"name":"British journal of rheumatology","volume":"37 10","pages":"1110-7"},"PeriodicalIF":0.0,"publicationDate":"1998-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20736899","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-beta2-glycoprotein I, anti-prothrombin and anticardiolipin antibodies in a longitudinal study of patients with systemic lupus erythematosus and the antiphospholipid syndrome.","authors":"M Inanç,&nbsp;S Donohoe,&nbsp;C T Ravirajan,&nbsp;E L Radway-Bright,&nbsp;I Mackie,&nbsp;S Machin,&nbsp;D A Isenberg","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objective: </strong>To determine anti-beta2 glycoprotein-I (anti-beta2GPI) and anti-prothrombin (anti-ProT) antibody levels, and the IgG subclass distribution of anti-beta2GPI antibodies, in serial samples from patients with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS) having initial or recurrent thrombotic/neurological (T/N) events during the study period. To investigate the correlations between these antibodies and beta2GPI antigen, anticardiolipin antibody (aCL), anti-double-stranded (ds) DNA, C3 levels and disease activity.</p><p><strong>Methods: </strong>Fifty serum samples were identified from seven patients with SLE who had had T/N events during the follow-up from a cohort under long-term follow-up. IgG anti-beta2GPI, anti-ProT, aCL, IgG subclasses of anti-beta2GPI and beta2GPI antigen levels were determined by ELISA. Corresponding disease activity [British Isles Lupus Assessment Group (BILAG)], anti-dsDNA and C3 levels were compared.</p><p><strong>Results: </strong>IgG anti-beta2GPI antibody levels were elevated in six of the patients before and after the T/N events with less marked fluctuations than aCL antibody levels. The predominant subclass of anti-beta2GPI antibodies was IgG2 before and after the T/N events. IgG anti-ProT antibodies were negative in all cases. There was a significant but weak correlation between anti-beta2GPI and aCL antibodies. No correlation was found between disease activity and IgG anti-beta2GPI antibody and beta2GPI antigen levels. There were fluctuations in beta2GPI antigen levels and a trend to increase after T/N events was observed in some patients.</p><p><strong>Conclusion: </strong>Most of the patients with a T/N event during the study period had IgG anti-beta2GPI, but not IgG anti-ProT antibodies. Many IgG aCL-negative samples were found to have IgG anti-beta2GPI activity during the follow-up period. The predominant subclass of IgG anti-beta2GPI was IgG2, which may have importance in the pathogenesis of APS. beta2GPI antigen levels were found to be increased in some patients with SLE after T/N events. IgG anti-beta2GPI antibodies may be used as an adjunctive marker of future T/N events in patients with SLE and APS with aCL antibodies and lupus anticoagulant.</p>","PeriodicalId":9307,"journal":{"name":"British journal of rheumatology","volume":"37 10","pages":"1089-94"},"PeriodicalIF":0.0,"publicationDate":"1998-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20736972","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fatigue in rheumatoid arthritis: the role of self-efficacy and problematic social support.","authors":"R P Riemsma,&nbsp;J J Rasker,&nbsp;E Taal,&nbsp;E N Griep,&nbsp;J M Wouters,&nbsp;O Wiegman","doi":"10.1093/rheumatology/37.10.1042","DOIUrl":"https://doi.org/10.1093/rheumatology/37.10.1042","url":null,"abstract":"<p><strong>Objective: </strong>To examine the relationship of fatigue in people with rheumatoid arthritis (RA) with self-efficacy, positive and problematic aspects of social support, and demographic and disease-related variables.</p><p><strong>Method: </strong>Out-patients with at least 5 yr RA were studied. Fatigue was measured with a visual analogue scale. Other variables included were: positive social support [Social Support List-Interactions (SSL12-I)] and problematic social support; self-efficacy towards coping with RA and towards mobilizing support; health status (Dutch-AIMS2); and laboratory tests: erythrocyte sedimentation rate (ESR), haemoglobin (Hb) and rheumatoid factor (RF); and disease duration.</p><p><strong>Results: </strong>A total of 229 out-patients were included. Fatigue correlated with all scales of the Dutch-AIMS2: with pain, physical function and affect (P < 0.001). There was no significant correlation with social support, but there was a highly significant correlation of fatigue with problematic social support (P < 0.001). Both forms of self-efficacy correlated strongly with fatigue: patients with high self-efficacy expectations towards coping with RA, and towards mobilizing the social network (P < 0.001), had less fatigue. In the regression analysis to explain the variation in fatigue, only pain, self-efficacy expectations towards coping with RA, and towards asking for help and problematic social support remained significant.</p><p><strong>Conclusions: </strong>Fatigue can to a large extent (37%) be explained by pain, self-efficacy towards coping with RA, and towards asking for help and problematic social support. It is known that self-efficacy can be enhanced by self-management courses and it may thus be possible to improve fatigue.</p>","PeriodicalId":9307,"journal":{"name":"British journal of rheumatology","volume":"37 10","pages":"1042-6"},"PeriodicalIF":0.0,"publicationDate":"1998-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1093/rheumatology/37.10.1042","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20735810","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alteration of central serotonin modifies onset and severity of adjuvant-induced arthritis in the rat.","authors":"M S Harbuz,&nbsp;O Marti,&nbsp;S L Lightman,&nbsp;D S Jessop","doi":"10.1093/rheumatology/37.10.1077","DOIUrl":"https://doi.org/10.1093/rheumatology/37.10.1077","url":null,"abstract":"<p><strong>Objective: </strong>Previous studies have determined that depletion of serotonin reduces the severity of hind-paw inflammation in adjuvant-induced arthritis (AA) in the rat. We wished to (i) test the hypothesis that this effect may be mediated, at least in part, through a central mechanism and (ii) to investigate further the pro-inflammatory role of serotonin we determined whether increasing serotonin using a selective serotonin reuptake inhibitor (SSRI), to increase serotonin availability at the active site of release, would increase inflammation.</p><p><strong>Methods: </strong>(i) Serotonin was depleted in the brain of rats with the selective neurotoxin 5'7'-dihydroxytryptamine. (ii) Rats were treated with an SSRI on days 10, 11 and 12 following adjuvant injection. Hind-paw inflammation was determined with plethysmometry as an index of severity of inflammation, and brain, pituitaries and blood were collected for assessment of changes in the hypothalamo -pituitary adrenal (HPA) axis.</p><p><strong>Results: </strong>(i) Serotonin depletion significantly reduced hind-paw inflammation. (ii) SSRI-treated animals developed hind-paw inflammation sooner, and the severity was increased compared to vehicle-treated AA rats. The changes in the HPA axis associated with inflammation were partly reversed by this treatment.</p><p><strong>Conclusion: </strong>These data suggest a pro-inflammatory role for central serotonin in this disease model and indicate that treatment with SSRIs may exacerbate the development of inflammation.</p>","PeriodicalId":9307,"journal":{"name":"British journal of rheumatology","volume":"37 10","pages":"1077-83"},"PeriodicalIF":0.0,"publicationDate":"1998-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1093/rheumatology/37.10.1077","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20736970","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparison of clinical and self-reported diagnoses for participants on a community-based arthritis self-management programme.","authors":"J H Barlow,&nbsp;A P Turner,&nbsp;C C Wright","doi":"10.1093/rheumatology/37.9.985","DOIUrl":"https://doi.org/10.1093/rheumatology/37.9.985","url":null,"abstract":"<p><strong>Objective: </strong>With the advent of community-based arthritis education programmes, it is important to determine the accuracy of participants' self-reported diagnoses. The purpose of this study was to determine the level of agreement between general practitioner (GP)-recorded and self-reported diagnoses of participants attending an Arthritis Self-Management Programme (ASMP).</p><p><strong>Methods: </strong>Participants enrolling on the ASMP were asked to (a) identify their type of arthritis via a self-administered postal questionnaire and (b) obtain a written confirmation of their diagnosis from their GP. The sample (n = 613) comprised mainly women (83%) with a mean age of 58.8 yr (S.D. 12.6) and a mean disease duration of 15.4 yr (S.D. 12.5).</p><p><strong>Results: </strong>Participants' self-reported diagnoses were confirmed by GPs in 534 cases [87.1%, 95% confidence interval (CI): 84.4 89.8%]. Confirmed diagnoses were reported by 86.9% (95% CI: 83.1-90.7%) of those with osteoarthritis (OA) and 96.1% (95% CI: 93.6 98.6%) of those with rheumatoid arthritis (RA). The concordance rate for all other types of arthritis combined was lower at 60.5% (95% CI: 49.5-71.5%). There were no significant differences with respect to age, gender, education, physical functioning, duration of disease and number of GP visits between those who correctly identified their type of arthritis and those who did not.</p><p><strong>Conclusions: </strong>This study suggests that the majority of RA and OA participants attending an arthritis education programme can correctly identify their specific type of arthritis.</p>","PeriodicalId":9307,"journal":{"name":"British journal of rheumatology","volume":"37 9","pages":"985-7"},"PeriodicalIF":0.0,"publicationDate":"1998-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1093/rheumatology/37.9.985","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20695885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Female sex hormones at the onset of systemic lupus erythematosus affect survival.","authors":"M J Rood,&nbsp;E A Van Der Velde,&nbsp;R Ten Cate,&nbsp;F C Breedveld,&nbsp;T W Huizinga","doi":"10.1093/rheumatology/37.9.1008","DOIUrl":"https://doi.org/10.1093/rheumatology/37.9.1008","url":null,"abstract":"<p><p>Female sex hormones affect susceptibility to systemic lupus erythematosus (SLE). To determine the effect of female sex hormones at onset of SLE on the survival of these patients, a retrospective survey was performed. The charts of 168 female SLE patients were evaluated to study the disease course, in particular the presence and kind of SLE criteria. Patients were classified as either belonging to the 'high female sex hormone at onset (HH)' or 'low female sex hormone at onset (LH)' group according to age at diagnosis. The statistics of the Dutch population, matched for age, were used to control for differences in life expectancy in these groups. A Cox regression model revealed that the relative mortality risk of HH patients vs HH controls was 4.2 times higher than the relative mortality risk of LH patients compared to LH controls. No differences in the frequency of SLE criteria between HH and LH patients were found that could explain the observed difference in mortality risk.</p>","PeriodicalId":9307,"journal":{"name":"British journal of rheumatology","volume":"37 9","pages":"1008-10"},"PeriodicalIF":0.0,"publicationDate":"1998-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1093/rheumatology/37.9.1008","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20695889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regaining self-control--regulation and immunotherapy.","authors":"J D Isaacs,&nbsp;H Waldmann","doi":"10.1093/rheumatology/37.9.926","DOIUrl":"https://doi.org/10.1093/rheumatology/37.9.926","url":null,"abstract":"","PeriodicalId":9307,"journal":{"name":"British journal of rheumatology","volume":"37 9","pages":"926-9"},"PeriodicalIF":0.0,"publicationDate":"1998-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1093/rheumatology/37.9.926","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20697114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Successful treatment of gastrointestinal vasculitis due to systemic lupus erythematosus with intravenous pulse cyclophosphamide: a clinical case report and review of the literature.","authors":"B Grimbacher,&nbsp;M Huber,&nbsp;J von Kempis,&nbsp;P Kalden,&nbsp;M Uhl,&nbsp;G Köhler,&nbsp;H E Blum,&nbsp;H H Peter","doi":"10.1093/rheumatology/37.9.1023","DOIUrl":"https://doi.org/10.1093/rheumatology/37.9.1023","url":null,"abstract":"<p><p>Gastrointestinal vasculitis in systemic lupus erythematosus (SLE) is quite rare and almost always accompanied by evidence of active disease in other organs, although occasionally it may be the presenting feature of the disease. Gastrointestinal involvement in SLE may present as lupus peritonitis, non-necrotizing pancreatitis, gastrointestinal vasculitis or surgical abdomen. Here we report a severe case of SLE which presented initially with fever of unknown origin. Severe distress, abdominal pain, the presence of occult blood in the stool and high acute-phase proteins were explained by a lupus peritonitis and intestinal vasculitis resembling inflammatory bowel disease. Whereas high-dose prednisone treatment did not prevent a severe relapse, we observed a sustained remission following i.v. cyclophosphamide pulse therapy. In the literature, only two similar cases are reported: one died despite a change in the therapy of a bowel perforation; our case was the second that improved under pulse cyclophosphamide. We suggest the use of cyclophosphamide after failure of steroids early in the course of SLE gastrointestinal vasculitis to prevent devastating complications.</p>","PeriodicalId":9307,"journal":{"name":"British journal of rheumatology","volume":"37 9","pages":"1023-8"},"PeriodicalIF":0.0,"publicationDate":"1998-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1093/rheumatology/37.9.1023","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20695826","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}