Annals of the rheumatic diseases (Ann Rheum Dis )

Publisher: Arthritis and Rheumatism Council for Research in Great Britain and the Commonwealth, BMJ Publishing Group

Description

First published in 1939, Annals of the Rheumatic Diseases (ARD) features original work on all aspects of rheumatology and disorders of the connective tissue. Topical leaders and reviews are commissioned to address the wider aspects of rheumatology. Fully international, Annals of the Rheumatic Diseases publishes clinical, epidemiological and laboratory reports, hypothesis articles and clinical teaching (including diagnostic radiology cases and Lesson of the Month). Concise scientific communication is encouraged and peer-reviewed proceedings of international meetings are featured within monthly issues.

  • Impact factor
    8.11
  • 5-year impact
    6.96
  • Cited half-life
    5.30
  • Immediacy index
    2.19
  • Eigenfactor
    0.07
  • Article influence
    2.12
  • Website
    Annals of the Rheumatic Diseases website
  • Other titles
    Annals of the rheumatic diseases (Online)
  • ISSN
    1468-2060
  • OCLC
    41233919
  • Material type
    Document, Periodical, Internet resource
  • Document type
    Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

BMJ Publishing Group

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 6 months embargo
  • Conditions
    • On author or institutional server only
    • Publisher copyright and source must be acknowledged
    • Must link to publisher version
    • Publisher's version/PDF cannot be used
    • Accepted version may be placed on PubMed Central and mirror sites after 12 months from publication
  • Classification
    ​ yellow

Publications in this journal

  • Annals of the rheumatic diseases 05/2014; 73(5):791-3.
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    ABSTRACT: S100A4 is a calcium binding protein with regulatory functions in cell homeostasis, proliferation and differentiation that has been shown to promote cancer progression and metastasis. In the present study, we evaluated the role of S100A4 in fibroblast activation in systemic sclerosis (SSc). The expression of S100A4 was analysed in human samples, murine models of SSc and in cultured fibroblasts by real-time PCR, immunohistochemistry and western blot. The functional role of S100A4 was evaluated using siRNA, overexpression, recombinant protein and S100A4 knockout (S100A4(-/-)) mice. Transforming growth factor β (TGF-β) signalling was assessed by reporter assays, staining for phosphorylated Smad2/3 and analyses of target genes. The expression of S100A4 was increased in SSc skin and in experimental fibrosis in a TGF-β/Smad-dependent manner. Overexpression of S100A4 or stimulation with recombinant S100A4 induced an activated phenotype in resting normal fibroblasts. In contrast, knockdown of S100A4 reduced the pro-fibrotic effects of TGF-β and decreased the release of collagen. S100A4(-/-) mice were protected from bleomycin-induced skin fibrosis with reduced dermal thickening, decreased hydroxyproline content and lower myofibroblast counts. Deficiency of S100A4 also ameliorated fibrosis in the tight-skin-1 (Tsk-1) mouse model. We characterised S100A4 as a downstream mediator of the stimulatory effects of TGF-β on fibroblasts in SSc. TGF-β induces the expression of S100A4 to stimulate the release of collagen in SSc fibroblasts and induce fibrosis. Since S100A4 is essentially required for the pro-fibrotic effects of TGF-β and neutralising antibodies against S100A4 are currently evaluated, S100A4 might be a candidate for novel antifibrotic therapies.
    Annals of the rheumatic diseases 04/2014;
  • Annals of the rheumatic diseases 04/2014;
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    ABSTRACT: To study clinical predictors for radiographic progression after 1 year in an early rheumatoid arthritis (RA) trial. In the SWEFOT trial population, disease modifying antirheumatic drug (DMARD) naïve RA patients started methotrexate; 3-month responders (DAS28 <3.2) continued (n=147), while non-responders were randomised to addition of sulfasalazine+hydroxychloroquine (n=130) or infliximab (n=128). X-rays were scored by the Sharp-van der Hejde score (SHS) method and radiographic progression was defined as a ≥5 increase after 1 year. Potential baseline predictors of radiographic progression were tested using multivariable logistic regression, adjusted for potential confounders. 79 of 311 patients with available radiographs at baseline and follow-up had radiographic progression. The following baseline parameters were independent predictors of radiographic progression at 1 year: baseline erosions (adjusted OR=2.29, 95% CI 1.24 to 4.24), erythrocyte sedimentation rate (adjusted OR per tertile increase=1.72, 95% CI 1.12 to 2.65) and C-reactive protein (adjusted OR per tertile increase=1.52, 95% CI 1.03 to 2.26). Current smoking was an independent predictor of radiographic progression (adjusted OR=2.17, 95% CI 1.06 to 4.45). These results remained after further adjustment for treatment strategy. Three-dimensional matrix including current smoking status, erosions and C-reactive protein tertiles showed a 12-63% risk gradient from patients carrying none compared with all predictors. Rheumatoid factor (RF)/anti-cyclic citrullinated peptide (anti-CCP) positivity did not significantly predict radiographic progression using SHS increase ≥5 as cut-off. In a secondary exploratory analysis using cut-off >1, both RF and anti-CCP positivity were significant predictors in the unadjusted, but not the adjusted analyses. The other parameters also remained significant using this lower cut-off. In addition to previously described predictors, we identified smoking as a strong independent risk factor for radiographic progression in early RA. NCT00764725.
    Annals of the rheumatic diseases 04/2014;
  • Annals of the rheumatic diseases 04/2014;
  • Annals of the rheumatic diseases 04/2014;
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    ABSTRACT: The occurrence of polymyositis (PM) and dermatomyositis (DM) in the general population is largely unknown and unbiased data on clinical and laboratory features in PM/DM are missing. Here, we aim to identify and characterise every PM/DM patient living in southeast Norway (denominator population 2.64 million), 2003-2012. Due to the structure of the Norwegian health system, all patients with PM/DM are followed at public hospitals. Hence, all public hospital databases in southeast Norway were screened for patients having ICD-10 codes compatible with myositis. Manual chart review was then performed to identify all cases meeting the Peter & Bohan and/or Targoff classification criteria for PM/DM. The ICD-10 search identified 3160 potential myositis patients, but only 208/3160 patients met the Peter & Bohan criteria and 230 the Targoff criteria (100 PM, 130 DM). With 56 deaths during the observation period, point prevalence of PM/DM was calculated to 8.7/100 000. Estimated annual incidences ranged from 6 to 10 /1 000 000, with peak incidences at 50-59 (DM) and 60-69 years (PM). Myositis specific antibodies (Jo-1, PL-7, PL-12, signal recognition particle (SRP) and Mi-2) were present in 53% (109/204), while 137/163 (87%) had pathological muscle MRI. Frequent clinical features included myalgia (75%), arthritis (41%) dyspnoea (62%) and dysphagia (58%). Positive anti-Jo-1, present in 39% of DM and 22% of PM cases, was associated with dyspnoea, arthritis and mechanic hands. Our data indicate that the population prevalence of PM/DM in Caucasians is quite low, but underscores the complexity and severity of the disorders.
    Annals of the rheumatic diseases 04/2014;
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    ABSTRACT: To compare arterial haemodynamics in adults with long-term juvenile idiopathic arthritis (JIA) to that of healthy controls, and explore the influence of traditional cardiovascular risk factors and disease characteristics on arterial haemodynamics plus coronary artery calcification. 87 JIA patients (median age 38.4 years) with persistently active disease at least 15 years after disease onset (registered by longitudinal follow-up), were re-examined after median 29 years and compared with 87 matched controls. Arterial haemodynamics were characterised by arterial stiffness and blood pressure. Sphygmocor was used to measure the arterial stiffness markers pulse wave velocity (PWV) and augmentation index (AIx). Coronary calcification was assessed by CT. Compared to controls, patients had significantly higher PWV (7.2 vs 6.9 m/s, p=0.035), and systolic and diastolic blood pressure (SBP, p=0.050 and DBP, p=0.029). AIx was numerically higher in the patients compared to the controls, but no statistically significant difference was found. Coronary calcification was present in 22 (26%) of the patients. Daily smoking was more frequent (p=0.043), and insulin resistance was higher (p=0.034) in patients than controls.In patients, DBP, but no disease variables were determinants of PWV. Disease variables as well as traditional cardiovascular risk factors were associated with higher AIx, DBP and the presence of coronary calcification. JIA patients with long-term active disease had altered arterial haemodynamics compared with controls in our study. PWV was mainly determined by increased DBP, a parameter that again was associated with JIA disease and treatment variables.
    Annals of the rheumatic diseases 04/2014;
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    ABSTRACT: Smoking can induce autoantibodies in persons who are genetically predisposed to rheumatoid arthritis. We investigated the association between smoking and antiphospholipid antibodies (aPL) in systemic lupus erythematosus (SLE), a question not previously addressed. Further, we explored the relationship between smoking, aPL and vascular events (arterial and venous, VE). In this cross-sectional study, clinical evaluation and questionnaire data were collected from 367 prevalent SLE patients. At the same time, we measured aPL (anticardiolipin (aCL), anti-β2 glycoprotein-1 (aβ2GP1) antibodies IgG/IgM/IgA, and lupus anticoagulant (LA)), and a large set of other SLE-associated autoantibodies for comparison. Association analyses using logistic regression models with smoking, (ever, former and current with never as reference) and antibody status as outcome variable were performed. As a secondary outcome, we investigated the associations between aPL, smoking and VE. In multivariable-adjusted models ever, and in particular former, cigarette smoking was associated with the most pathogenic aPL; LA, aCL IgG and aβ2GP1 IgG. Other SLE-associated autoantibodies were not associated with smoking. The combination of smoking and aPL was strongly associated with VE. We noted a positive interaction between smoking-LA and smoking-'triple aPL' positivity for previous VE. We investigated a large set of commonly occurring autoantibodies in SLE, but only aPL were positively associated with a history of smoking. This association was especially apparent in former smokers. Among ever regular smokers who were aPL positive, we observed a strikingly high frequency of former VE. The underlying mechanisms and temporality between smoking, aPL and VE need further investigations.
    Annals of the rheumatic diseases 04/2014;
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    ABSTRACT: The Global Burden of Disease Study 2010 estimated the worldwide health burden of 291 diseases and injuries and 67 risk factors by calculating disability-adjusted life years (DALYs). Osteoporosis was not considered as a disease, and bone mineral density (BMD) was analysed as a risk factor for fractures, which formed part of the health burden due to falls. To calculate (1) the global distribution of BMD, (2) its population attributable fraction (PAF) for fractures and subsequently for falls, and (3) the number of DALYs due to BMD. A systematic review was performed seeking population-based studies in which BMD was measured by dual-energy X-ray absorptiometry at the femoral neck in people aged 50 years and over. Age- and sex-specific mean ± SD BMD values (g/cm(2)) were extracted from eligible studies. Comparative risk assessment methodology was used to calculate PAFs of BMD for fractures. The theoretical minimum risk exposure distribution was estimated as the age- and sex-specific 90th centile from the Third National Health and Nutrition Examination Survey (NHANES III). Relative risks of fractures were obtained from a previous meta-analysis. Hospital data were used to calculate the fraction of the health burden of falls that was due to fractures. Global deaths and DALYs attributable to low BMD increased from 103 000 and 3 125 000 in 1990 to 188 000 and 5 216 000 in 2010, respectively. The percentage of low BMD in the total global burden almost doubled from 1990 (0.12%) to 2010 (0.21%). Around one-third of falls-related deaths were attributable to low BMD. Low BMD is responsible for a growing global health burden, only partially representative of the real burden of osteoporosis.
    Annals of the rheumatic diseases 04/2014;
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    ABSTRACT: The metabolic syndrome (MetS) may contribute to the increased cardiovascular risk in systemic lupus erythematosus (SLE). We examined the association between MetS and disease activity, disease phenotype and corticosteroid exposure over time in patients with SLE. Recently diagnosed (<15 months) patients with SLE from 30 centres across 11 countries were enrolled into the Systemic Lupus International Collaborating Clinics (SLICC) Inception Cohort from 2000 onwards. Baseline and annual assessments recorded clinical, laboratory and therapeutic data. A longitudinal analysis of factors associated with MetS in the first 2 years of follow-up was performed using random effects logistic regression. We studied 1150 patients with a mean (SD) age of 34.9 (13.6) years and disease duration at enrolment of 24.2 (18.0) weeks. In those with complete data, MetS prevalence was 38.2% at enrolment, 34.8% at year 1 and 35.4% at year 2. In a multivariable random effects model that included data from all visits, prior MetS status, baseline renal disease, SLICC Damage Index >1, higher disease activity, increasing age and Hispanic or Black African race/ethnicity were independently associated with MetS over the first 2 years of follow-up in the cohort. MetS is a persistent phenotype in a significant proportion of patients with SLE. Renal lupus, active inflammatory disease and damage are SLE-related factors that drive MetS development while antimalarial agents appear to be protective from early in the disease course.
    Annals of the rheumatic diseases 04/2014;
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    ABSTRACT: To develop and validate rheumatoid arthritis (RA) risk models based on family history, epidemiologic factors and known genetic risk factors. We developed and validated models for RA based on known RA risk factors, among women in two cohorts: the Nurses' Health Study (NHS, 521 RA cases and 517 controls) and the Epidemiological Investigation of RA (EIRA, 1244 RA cases and 971 controls). Model discrimination was evaluated using the area under the receiver operating characteristic curve (AUC) in logistic regression models for the study population and for those with positive family history. The joint effect of family history with genetics, smoking and body mass index (BMI) was evaluated using logistic regression models to estimate ORs for RA. The complete model including family history, epidemiologic risk factors and genetics demonstrated AUCs of 0.70 for seropositive RA in NHS and 0.77 for anti-citrullinated protein antibody (ACPA)-positive RA in EIRA. Among women with positive family history, discrimination was excellent for complete models for seropositive RA in NHS (AUC 0.83) and ACPA-positive RA in EIRA (AUC 0.83). Positive family history, high genetic susceptibility, smoking and increased BMI had an OR of 21.73 for ACPA-positive RA. We developed models for seropositive and seronegative RA phenotypes based on family history, epidemiological and genetic factors. Among those with positive family history, models using epidemiologic and genetic factors were highly discriminatory for seropositive and seronegative RA. Assessing epidemiological and genetic factors among those with positive family history may identify individuals suitable for RA prevention strategies.
    Annals of the rheumatic diseases 03/2014;
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    ABSTRACT: Patients with rheumatoid arthritis (RA) have an increased risk of certain solid cancers, in particular lung cancer, compared to the general population. Treatment with tumour necrosis factor (TNF) inhibitors (TNFi) may further enhance this risk. To compare the risk of solid cancer in patients with RA treated with TNFi to that in patients treated with non-biologic (synthetic) disease modifying antirheumatic drugs (sDMARDs). Patients with a physician diagnosis of RA enrolled in the British Society for Rheumatology Biologics Register, a national prospective cohort study established in 2001 to monitor the long-term safety of TNFi, were followed via record linkage with the national cancer registries until first solid cancer, death, for 5 years, or until 2011. Rates of solid cancers in 11 767 patients without prior cancer who received TNFi were compared to those in 3249 patients without prior cancer treated with sDMARDs. 427 solid cancers were reported in 52 549 patient-years follow-up for the TNFi group (81 (95% CI 74 to 89) per 10 000 patient-years) and 136 cancers were reported in 11 672 patient-years in the sDMARD cohort (117 (95% CI 98 to 138) per 10 000 patient-years). After adjusting for differences in baseline characteristics there was no difference in risk of solid cancer for TNFi compared to sDMARD treated patients: HR 0.83 (95% CI 0.64 to 1.07). There was no difference in the relative risk of cancer for any of the individual TNFi drugs. The addition of TNFi to sDMARD does not alter the risk of cancer in RA patients selected for TNFi in the UK.
    Annals of the rheumatic diseases 03/2014;
  • Annals of the rheumatic diseases 03/2014;
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    ABSTRACT: To assess the efficacy of methotrexate (MTX) in decreasing pain and inflammation in symptomatic knee osteoarthritis (OA). One hundred and forty-four patients with primary knee OA were randomised in a 1:1 ratio to receive up to 25 mg/week oral MTX (n=72) or placebo (n=72) for 28 weeks. Outcome measures included reduction in pain and inflammation and improvements in physical function scores. Pain was assessed using the visual analogue pain scale, (VAS, 0-100 mm). Functional assessment was performed using the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) and activities of daily living (ADL) scores. Synovitis was detected clinically and by ultrasound imaging at baseline and at the end of the study. There was a clinically relevant reduction in the intervention group compared with the placebo group for knee pain, physical function and ADL scores at 28 weeks. The mean difference between treatment arms (95% CI) was 11.4 (2.8 to 20.0), p=0.009; 9.5 (3.7 to 15.3) p=0.001 and 1.2 (0.1 to 2.3), p=0.032, respectively. Furthermore, a clinically relevant reduction in synovitis (both clinically and by ultrasound) was noted in the MTX group compared with the placebo group at 28 weeks. The proportion of patients who had a reduction in VAS of >20 mm was significantly higher in the MTX group (n=38) 53% than in the placebo group (n=17) 24%, p=0.018. MTX significantly reduced pain and improved synovitis. There was a significant improvement in physical function. MTX may be a therapeutic option in the treatment of pain and inflammation related to knee OA. NCT01927484.
    Annals of the rheumatic diseases 03/2014;
  • Annals of the rheumatic diseases 03/2014;
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    ABSTRACT: Erdheim-Chester disease (ECD) is a rare form of histiocytosis characterised by uncontrolled chronic inflammation. The oncogenic BRAF(V600E) mutation has been reported in biopsies in 19 out of 37 patients with ECD from the largest published cohort, but never found in the patients' peripheral blood. Also, the role of the mutation in the pathogenesis of the disease has not been elucidated yet. BRAF(V600E) has been associated with oncogene-induced senescence (OIS), a protective mechanism against oncogenic events, characterised by the induction of proinflammatory pathways. We verified the BRAF status in biopsies and peripheral blood from 18 patients with ECD from our cohort and matched controls by means of immunohistochemistry and of an ultrasensitive assay, based on the combination of a locked nucleic acid PCR and pyrosequencing. Droplet digital PCR was used to confirm the findings. We also evaluated the presence of senescence markers in ECD histiocytes. BRAF(V600E) mutation was present in all the biopsy and peripheral blood samples from patients with ECD and in none of the controls. ECD histiocytes and a fraction of circulating monocytes from patients with ECD showed signs of a constitutive activation of the MAPK pathway. Moreover, BRAF-mutated histiocytes expressed markers of OIS. The oncogenic BRAF(V600E) mutation is present in biopsies and in the peripheral blood from all patients with ECD who were evaluated and is associated with OIS. These findings have significant implications for the pathogenesis, diagnosis and treatment of ECD.
    Annals of the rheumatic diseases 03/2014;
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    ABSTRACT: Hand exercises are recommended for patients with hand osteoarthritis (HOA), though evidence for their effect is conflicting. To evaluate, in a randomised controlled trial, the effect of HOA information plus home-based hand exercises (exercise group) compared with information only (control group) in women with HOA. Interventions were delivered by two occupational therapists. Exercise group participants received eight follow-up calls over the 3-month study and recorded adherence, pain after exercises and adverse events in a diary. Primary outcome was activity performance measured after 3 months by the Patient-Specific Functional Scale (PSFS), with a range of 0-10. Secondary outcomes were measurements of hand function, disease activity, symptoms and number of responders to treatment according to the OMERACT-OARSI criteria. Of 80 women randomised (40 : 40) (mean age (SD) 60.8 years (7.0)), follow-up was 89% (n=71). An intention-to-treat analysis was performed. The adjusted mean difference for the exercise versus control group was 1.4 points (95% CI 0.6 to 2.2, effect size 1.0) for the PSFS score. Thirteen patients in the exercise group versus three participants in the control group reached a positive minimal clinical important difference of 2.2 points in the PSFS total score, while none versus two, respectively, had a negative change (p=0.007). For secondary outcomes, significant mean differences were found in grip strength and thumb web space, in fatigue, joint pain and the Functional Index for HOA activity performance scores. Sixteen exercise-group participants fulfilled the OMERACT-OARSI response criteria versus two control-group participants (p<0.001). Hand exercises were well tolerated and significantly improved activity performance, grip strength, pain and fatigue in women with HOA. ISRTCN79019063.
    Annals of the rheumatic diseases 03/2014;
  • Annals of the rheumatic diseases 03/2014;
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    ABSTRACT: To assess the accuracy of dual-energy CT (DECT) for diagnosing gout, and to explore whether it can have any impact on clinical decision making beyond the established diagnostic approach using polarising microscopy of synovial fluid (diagnostic yield). Diagnostic single-centre study of 40 patients with active gout, and 41 individuals with other types of joint disease. Sensitivity and specificity of DECT for diagnosing gout was calculated against a combined reference standard (polarising and electron microscopy of synovial fluid). To explore the diagnostic yield of DECT scanning, a third cohort was assembled consisting of patients with inflammatory arthritis and risk factors for gout who had negative synovial fluid polarising microscopy results. Among these patients, the proportion of subjects with DECT findings indicating a diagnosis of gout was assessed. The sensitivity and specificity of DECT for diagnosing gout was 0.90 (95% CI 0.76 to 0.97) and 0.83 (95% CI 0.68 to 0.93), respectively. All false negative patients were observed among patients with acute, recent-onset gout. All false positive patients had advanced knee osteoarthritis. DECT in the diagnostic yield cohort revealed evidence of uric acid deposition in 14 out of 30 patients (46.7%). DECT provides good diagnostic accuracy for detection of monosodium urate (MSU) deposits in patients with gout. However, sensitivity is lower in patients with recent-onset disease. DECT has a significant impact on clinical decision making when gout is suspected, but polarising microscopy of synovial fluid fails to demonstrate the presence of MSU crystals.
    Annals of the rheumatic diseases 03/2014;

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