Clinical and experimental rheumatology (CLIN EXP RHEUMATOL)

Journal description

Clinical and Experimental Rheumatology is a bi-monthly journal which publishes original papers on clinical or experimental research pertinent to the rheumatic diseases; work on connective tissue diseases and other immune disorders also are within the journal's scope.

Current impact factor: 2.72

Impact Factor Rankings

2016 Impact Factor Available summer 2017
2014 / 2015 Impact Factor 2.724
2013 Impact Factor 2.973
2012 Impact Factor 2.655
2011 Impact Factor 2.148
2010 Impact Factor 2.358
2009 Impact Factor 2.396
2008 Impact Factor 2.364
2007 Impact Factor 2.27
2006 Impact Factor 2.189
2005 Impact Factor 2.366
2004 Impact Factor 1.504
2003 Impact Factor 1.919
2002 Impact Factor 1.284
2001 Impact Factor 1.614
2000 Impact Factor 1.638
1999 Impact Factor 1.348
1998 Impact Factor 1.27
1997 Impact Factor 1.152
1996 Impact Factor 0.925
1995 Impact Factor 0.987
1994 Impact Factor 1.342
1993 Impact Factor 1.59
1992 Impact Factor 1.481

Impact factor over time

Impact factor
Year

Additional details

5-year impact 2.43
Cited half-life 6.40
Immediacy index 0.34
Eigenfactor 0.01
Article influence 0.57
Website Clinical & Experimental Rheumatology website
Other titles Clinical and experimental rheumatology, Rheumatology
ISSN 0392-856X
OCLC 9404208
Material type Periodical
Document type Journal / Magazine / Newspaper

Publications in this journal

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    ABSTRACT: Objectives: To evaluate the associations between objectively measured gastroesophageal involvement using high-resolution manometry and 24- hour impedance-pH study, and clinical presentations in systemic sclerosis (SSc) patients. Methods: This cross-sectional study was conducted in University of Malaya Medical Centre (UMMC) with 31 consecutive SSc patients recruited into this study. Clinical symptoms of gastroesophageal involvement, high-resolution impedance-manometry and 24-hour impedance-pH monitoring were assessed. Their associations with serological features and other organ involvement were evaluated. Results: Twenty-five (80.6%) patients had gastroesophageal reflux disease (GORD) symptoms, mainly heartburn (45.1%), regurgitation (32.2%) and dysphagia (29%). Using manometry, oesophageal dysmotility was detected in 24 (88.9%) patients, while hypotensive lower oesophageal sphincter (LOS) was observed in 17 (63%) patients. 21 (84%) patients had GORD based on pH study. Hypotensive LOS was significantly associated with presence of digital ulcers. The main gastroesophageal symptoms were absent in majority of the SSc patients including in those with severe gastroesophageal manifestations demonstrating failed peristalsis >75%, hypotensive LOS, Demeester score >200 and acid reflux >200 per day. Demeester score >200 is associated with severity of GORD symptoms. Demeester score >200 was also associated with restrictive lung pattern (p=0.001). Significant association between GORD severity (daily number of acid reflux episodes >200) and pulmonary fibrosis was seen (p=0.030). Conclusions: The presence and severity of gastroesophageal symptoms may not accurately reflect the seriousness of oesophageal involvement. GORD severity is associated with presence of restrictive lung pattern and pulmonary fibrosis. Oesophageal manometry and 24-hour pH study should be considered more frequently in the assessment of SSc patients.
    No preview · Article · Feb 2016 · Clinical and experimental rheumatology
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    ABSTRACT: Objectives: Impairment of methylene tetrahydrofolate reductase (MTHFR), a key enzyme in the folate metabolism, results in an elevated plasma level of homocysteine, considered an independent risk factor for cardiovascular (CV) disease. Rheumatoid arthritis (RA) is a chronic inflammatory disease associated with increased risk of CV death. Polymorphisms in the MTHFR gene increase the frequency of CV disease in RA. The aim of this study was to determine the expression of MTHFR gene in patients with RA, with and without ischaemic heart disease (IHD). Methods: Relative expression of MTHFR gene and beta-actin and GAPDH as housekeeping genes was quantified by quantitative real-time polymerase chain reaction. It was analysed by the comparative Ct (threshold cycle) method in peripheral blood from 26 Spanish patients with RA (12 with IHD and 14 without IHD) and 10 healthy controls. MTHFR expression level in RA patients was also assessed according to disease activity, rheumatoid factor (RF) and anti-cyclic citrullinated peptide (anti-CCP) antibodies status. Results: MTHFR expression was significantly reduced in patients with RA compared to controls (fold change = 0.85, p=0.029). It was especially true for RA patients with IHD (fold change= 0.79, p=0.021). However, no statistically significant relationship between MTHFR expression level in patients with RA and DAS28 CRP, DAS28 ESR, RF and anti-CCP status was observed. Conclusions: Patients with RA, in particular those with IHD, show a decreased expression of the MTHFR gene. This may support a potential implication of the transcriptional regulation of MTHFR in the pathogenesis of RA.
    No preview · Article · Feb 2016 · Clinical and experimental rheumatology
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    ABSTRACT: Objectives: The aim of this study was to determine whether adult IgA vasculitis patients who developed the disease at an older age differ from early-onset patients in terms of clinical features and outcomes. Methods: All consecutive adult patients who were diagnosed with IgA vasculitis between January 1997 and December 2014 were reviewed retrospectively. Patients who developed the disease at an older age (≥60 years; late-onset) were compared with those with an earlier onset of disease (<60 years; early-onset). Renal insufficiency was defined as an estimated glomerular filtration rate <60 ml/minute. Results: In total, 100 adult patients were diagnosed with IgA vasculitis (mean age, 45.61 ± 17.24 years), of whom 31 (31%) had late-onset disease. Compared to early-onset patients, late-onset patients were less likely to have a preceding upper respiratory tract infection (0/31, 0.0% vs. 14/69, 20.3%; p=0.004), and more likely to have renal involvement at presentation (27/31, 87.1% vs. 43/69, 62.3%; p=0.017). At the last follow-up visit, late-onset patients were more likely to have chronic renal insufficiency, including end-stage renal disease (18/28, 64.3% vs. 7/62, 11.3%; p=0.000). Multivariate Cox analysis revealed that late-onset was a significant risk factor for renal insufficiency at follow-up (hazard ratio, 16.980, 95% confidence intervals, 4.380-65.830; p=0.000). Conclusions: Patients with late-onset IgA vasculitis in adults exhibit distinct clinical features characterized by greater renal involvement and worse renal outcomes. Thus, watchful follow-up might be needed for adult IgA vasculitis patients, in particular those with late-onset disease.
    No preview · Article · Feb 2016 · Clinical and experimental rheumatology
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    ABSTRACT: Objectives: Data from a small series suggested that the Interleukin 1 beta (IL1ß) rs16944 polymorphism may be associated with severe renal involvement and persistent renal damage (renal sequelae) in Henoch-Schönlein purpura (HSP). To confirm this association, we assessed the largest cohort of Caucasian HSP patients ever considered for genetic studies. Methods: 338 Spanish HSP patients and 635 sex and ethnically matched controls were recruited in this study. All patients were required to have had at least 6 months' follow-up. Patients and controls were genotyped for IL1β rs16944 by TaqMan genotyping assay. Results: No differences between IL1β rs16944 genotype or allele frequencies were found either in the case/control study or when HSP patients were stratified according to the age at disease onset, presence of nephritis or gastrointestinal manifestations. Nevertheless, 4 (25%) of the 16 HSP patients who developed severe renal manifestations carried the TT genotype versus 29 (9%) of 322 who did not develop this complication (p=0.01, OR=5.48, 95% CI: 1.01-28.10). Accordingly, patients carrying the mutant T allele had an increased risk of developing severe nephropathy (p=0.016, OR=2.35, 95% CI: 1.09-5.07). Additionally, a significant increase of the TT genotype was observed in patients with persistent renal damage when compared with those patients without this complication (25% versus 8.6%, respectively; p=0.0035, OR=4.90, 95% CI: 1.26- 18.51). Moreover, renal sequelae were more common in patients carrying the mutant T allele (p=0.0076, OR=2.20, 95% CI: 1.17-4.14). Conclusions: Our results support that the IL1ß rs16944 polymorphism may be a potential marker of severe renal manifestations and renal sequelae in HSP.
    No preview · Article · Feb 2016 · Clinical and experimental rheumatology
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    ABSTRACT: Objectives: The kidneys are frequently involved in antineutrophil cytoplasmic autoantibody (ANCA) associated small-vessel vasculitis (AASVV). The pathological hallmark of ANCA-associated glomerulonephritis (AAGN) is a pauci-immune necrotising crescentic glomerulonephritis. The histopathology of AAGN may change during the course of the disease as a consequence of immunosuppressive therapy. Herein, we report the pathological evolution of a case of AAGN. Methods: We report a female presented with renal-limited AASVV, hypocomplementemia and nephrotic syndrome. The first renal biopsy revealed "crescentic" changes at presentation, but after treatment with immunosuppressive treatment, a second renal biopsy four years later showed "mixed" changes of AAGN and immune complex deposition mimicking a mesangial proliferative glomerulonephritis. A literature review was undertaken in order to understand these transformations and factors which determine the pathological transitions. Results: AAGN is commonly described as a pauci-immune necrotising crescentic glomerulonephritis, but immune complex depositions have been frequently identified under electronic microscopy and is associated with greater levels of proteinuria. Acute lesions such as fibrinoid necrosis or glomerular crescent may completely disappear or reduce significantly after immunosuppressive therapy, but chronic changes may increase over time. Conclusions: Based on our review and the illustration of this case, the initial histopathology of an AAGN and its active fibrinoid necrosis and cellular glomerular crescent may disappear or resolve after immunosuppressive therapy with resulting non-distinctive feature. Understanding the transition may facilitate the clinical diagnosis and provide further insight into this disease.
    No preview · Article · Feb 2016 · Clinical and experimental rheumatology
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    ABSTRACT: Objectives: A low C4 level is one of the hallmarks of mixed cryoglobulinaemia (MC). However, several reports suggest that other factors may be involved in C4 depletion. The C4 gene is located in a multiallelic CNV locus in the human MHC region. We studied the C4 gene copy number (GCN) and both C4A and C4B isotypes, as well as the presence of the hypofunctional C4A6 allotype (rs41315824) and C4A0 allotype (rs367709216) in 41 MC patients, 16 SLE patients and 78 healthy controls. Methods: GCN of the C4 gene were evaluated by real time PCR. C4A6 allotype (p.Arg458Trp) and ins 2-bp mutation in exon 29 were screened by primer extension. Correlation with clinical signs of the disease (cutaneous ulcers, peripheral neuropathy, GN, purpura, hepatitis) have been performed by cluster analysis, (K-means algorithm). Results: C4 GCN analysis showed that fewer MC patients had more than 2 copies of the C4A gene as well as a lower C4A gene-copy index (1.90 ± 0.54 vs. 2.21 ± 0.78) as compared to healthy controls. SNP rs41315824 analysis showed a significant increase in the frequency of the p.Arg458Trp (C4A6) variant in cryoglobulinaemic patients. Lastly, cluster analysis allowed us to identify two separate clusters of patients. The cluster that included patients with three or less C4 gene copies was found to have a greater prevalence of the most severe complications such as glomerulonephritis, neuropathy and severe cutaneous ulcers. Conclusions: These data suggest there may be a relationship between polymorphisms of the C4 gene and clinical presentation.
    No preview · Article · Feb 2016 · Clinical and experimental rheumatology
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    No preview · Article · Feb 2016 · Clinical and experimental rheumatology
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    ABSTRACT: Objectives: The purpose of this work is to evaluate the usefulness of 18F-fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT) imaging in management of IgG4-related disease (IgG4-RD) by retrospective analysis of PET/CT results in IgG4-RD patients. Methods: Twenty-six patients diagnosed with IgG4-RD according to Japanese diagnostic criteria who underwent 18F-FDG-PET/CT scans in the PLA General Hospital from January 2010 to May 2015 were enrolled in the study. Their clinical presentations and 18F-FDG-PET/CT findings were analysed. Results: A total of 26 patients (20 men; 6 women) with a mean age of 53.8 years (range 35-71 years) and mean treatment course of 7.1 months (range 0.33-72 months) who underwent 18F-FDG-PET/CT scans were analysed. CRP was relatively low in all patients (mean 0.79 mg/dl). 18F-FDG-PET/CT images confirmed that two or more organs were involved in all patients, and average SUV values for involved organs was 4.14 (range 0.30-8.78). Eleven patients were misdiagnosed with submandibular tumours, pancreatic cancer, pancreatitis, pulmonary interstitial fibrosis, retroperitoneal fibrosis or systemic vasculitis prior to 18F-FDG-PET/CT imaging. Conclusions: 18F-FDG-PET/CT imaging is a useful tool for the differential diagnosis of IgG4-RD, and for mapping involved organs, guiding biopsy, and monitoring treatment response.
    No preview · Article · Feb 2016 · Clinical and experimental rheumatology
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    No preview · Article · Feb 2016 · Clinical and experimental rheumatology
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    ABSTRACT: Objectives: The effectiveness of anakinra (interleukin-1 receptor antagonist) in early rheumatoid arthritis (RA) is unknown. We evaluated the efficacy of anakinra (combined with methotrexate) in a randomised clinical trial of early active RA patients. Methods: The Combination Anti-Rheumatic Drugs in Early RA-2 (CARDERA-2) trial was a randomised trial of early (duration <1 year) active RA. Patients were randomised to 12 months of: (1) methotrexate or (2) anakinra-methotrexate. Follow-up lasted 2 years. The primary outcome was erosive progression (changes from baseline in modified Larsen scores). Secondary outcomes were changes from baseline in disease activity score on a 28-joint count (DAS28), health assessment questionnaire (HAQ), and quality of life (EQ-5D) scores alongside ACR responder rates. Results: 154 patients received the allocated intervention (from 259 screened). Similar Larsen score progression was seen at 12 and 24 months in patients receiving anakinra-methotrexate (mean changes from baseline of 2.50 and 5.10, respectively) and methotrexate monotherapy (mean changes from baseline of 4.16 and 5.20, respectively). Lower improvements in DAS28 and HAQ scores were seen at all time-points in anakinra-methotrexate treated patients; these were significantly less at 24 months (DAS28 p=0.04; HAQ P=0.02). Significantly lower EQ-5D score increases were seen at 12 months with anakinra-methotrexate (p=0.03). Anakinra-methotrexate was associated with more serious adverse events compared with methotrexate monotherapy (11 vs. 6 patients), although this was not significant (p=0.59). Conclusions: Anakinra (combined with methotrexate) is not effective in early, active RA. It provided no clinical benefits beyond methotrexate monotherapy.
    No preview · Article · Feb 2016 · Clinical and experimental rheumatology
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    ABSTRACT: Objectives: To evaluate the efficacy of etoricoxib in patients with axial ankylosing spondyloarthritis (AS) refractory to traditional NSAIDs. Methods: This was an open label, multicentric, randomised, prospective (4 weeks with and open extension to 6 months), non-controlled study. Consecutive patients with axial AS refractory to traditional NSAID eligible for anti-TNF-α therapy were selected. The primary outcomes were the rate of patients with good clinical response (not eligible for anti-TNF-α therapy after etoricoxib) and the Assessment of Spondyloarthritis International Society response criteria for biologic therapies (ASASBIO) response at 4 weeks. Secondary outcomes included: ASAS20 and 40 responses, ASDAS-CRP response, BASDAI, BASFI, back and night back pain, global patient and physician assessment of the disease, and biologic parameters like C-reactive protein (CRP) at 2, 4 weeks and 6 months. Results: A total of 57 axial AS patients were recruited, 46 men, with mean age of 43 years. After 4 weeks of treatment, 26 patients (46%) achieved a good clinical response and 11 (20%) an ASASBIO response. These results at 24 weeks were 19 (33%) and 13 (23%) respectively. All individual clinical variables improved significantly after 4 weeks of treatment. CRP serum levels decreased after 4 weeks but reached no statistical significance, although 30% of patients showed a normalisation of CRP. Conclusions: Etoricoxib provided a clear clinical improvement in around a third of patients with axial AS refractory to traditional NSAIDs. Special care should be required when deciding to start anti-TNF-α therapy; it seems reasonable to keep in mind these results of etoricoxib treatment.
    No preview · Article · Jan 2016 · Clinical and experimental rheumatology
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    ABSTRACT: Objectives: To investigate the expression of a VH1-69-encoded idiotype, and the phenotypic and functional features of monoclonal B-cells from patients with type II mixed cryoglobulinaemia (MC) secondary to chronic hepatitis B virus (HBV) infection. Methods: B-cell immunophenotype and expression of a VH1-69-encoded idiotype were investigated by flow cytometry. B-cell proliferative responses to stimuli were investigated by the CFSE dilution assay. Results: Two out of five patients with chronic HBV studied had massive monoclonal expansion of VH1-69-expressing B-cells. These cells had the peculiar CD21low phenotype and low responsiveness to stimuli typical of the VH1-69-expressing B-cells commonly expanded in MC secondary to hepatitis C virus (HCV) infection. In both patients, anti-HBV therapy led to the regression of MC and of VH1-69+ B-cell expansion. Conclusions: VH1-69-encoded antibodies are known to preferentially recognise a variety of viral proteins including HCV E2, influenza A virus haemagglutinin and HIV gp41/gp120, and may serve as innate first line antiviral defense. Thus, like HCV, HBV may cause MC by protracted antigenic stimulation of VH1-69-expressing B-cells.
    No preview · Article · Jan 2016 · Clinical and experimental rheumatology
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    No preview · Article · Jan 2016 · Clinical and experimental rheumatology
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    ABSTRACT: Objectives: The purpose of this study was to evaluate and compare the diagnostic performance of lung ultrasound (US) in respect to high-resolution computed tomography (HRCT) findings in patients with connective tissue disease-associated interstitial lung disease (CTD-ILD). Methods: We searched the Pubmed, Embase, and Cochrane Library databases, and performed a meta-analysis on the diagnostic accuracy of lung US according to B-lines (comet tail sign) and on the correlation coefficients between lung US scores and HRCT Warrick scores in CTD-ILD patients. Results: Five studies that included a total of 349 patients were available for this meta-analysis. The pooled sensitivity and specificity of lung US were 91.5% (95% confidence interval [CI]: 84.5-96.0) and 81.3% (95% CI: 74.6-86.9), respectively. The positive likelihood ratio, negative likelihood ratio, and diagnostic odds ratio were 4.100 (2.133-7.879), 0.176 (0.006-0.363), and 34.73 (10.10-99.66), respectively. The area under the curve was 0.915 and the Q* index was 0.848, indicating a high diagnostic accuracy. When all four studies with systemic sclerosis were considered together, the pooled sensitivity and specificity of lung US were 89.5% (95% CI 80.3-95.3) and 79.6% (69.9-87.2), respectively. A significant correlation was found between lung US B-line scores and HRCT Warrick scores in CTD-ILD (correlation coefficient: 0.783; p-value <1 × 10-9). Conclusions: Our meta-analysis of published studies demonstrates that lung US has a high diagnostic accuracy, correlates well with HRCT findings, and plays an important role in the diagnosis of CTD-ILD.
    No preview · Article · Jan 2016 · Clinical and experimental rheumatology
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    No preview · Article · Jan 2016 · Clinical and experimental rheumatology
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    ABSTRACT: Objectives: TNF-α has been proved to be an effective target in rheumatoid arthritis treatment. So far, all the commercialised TNF-α antagonists function as passive immunotherapy. The aim of this study was to design a complex which can trigger active immunisation and overcome self-tolerance to elicit antibodies against murine TNF-α. Methods: The complex (KLH-TNF) was chemically synthesised by linking a selected peptide TNFα4-23 from murine soluble TNF-α to a carrier protein, keyhole limpet haemocyanin (KLH). We evaluated its safety and antibody eliciting performance. We also evaluated its disease-regulating ability on collagen-induced arthritis models. Furthermore, the immune cells responses were analysed by T cell proliferation assay and B cell memory experiments. Results: The complex was safe without cytotoxity. The anti-mTNF-α antibody titers of the KLH-TNF group were 400 times greater than the control groups (p<0.0001). The elicited antibodies could combine with soluble TNF-α. The antibody response was independent of autologous TNF-α and could be reinforced by booster immunisation. Moreover, the complex did not trigger T cell activation and B cell memory response against native TNF-α. In animal experiments, KLH-TNF immunized mice showed a lower arthritis score (p<0.001) and better weight gain (p<0.01). Histological evaluations showed milder inflammation and cartilage depletion. Conclusions: Active immunotherapy against cytokine TNF-α is feasible by conjugating cytokine peptide with carrier protein. The elicited antibodies could combine with the native TNF-α and inhibit its activity. Importantly, the antibody response is reversible and independent of autologous TNF-α.
    No preview · Article · Jan 2016 · Clinical and experimental rheumatology
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    ABSTRACT: Objectives: Enthesitis is an important clinical manifestation and is a diagnostic criterion for juvenile idiopathic enthesitis-related arthritis (JIA-ERA). Ultrasound (US) is a highly sensitive method of detection of enthesitis in adult spondyloarthropathies. However, since the data on JIA and the preformance of US compared to clinical examination is limited, we aimed to compare the accuracy of US and clinical examination in JIA-ERA. Methods: Patients with JIA-ERA (ILAR criteria) were enrolled in the study after consent. Besides data on disease variables, enthesitis was evaluated clinically as well as by ultrasound. Six entheseal sites (iliac crest, superior pole patella, inferior pole patella, tibial tuberosity, tendoachilles and plantar fascia) on both sides of the body were examined in each patient. Features of acute and chronic enthesitis were noted. Results: 360 entheseal sites in 30 male patients (26 positive for HLA-B27), with a median age of 16 years and median disease duration of 4 years were evaluated. Median Madrid Sonology Enthesitis Index (MSEI) was 2.0 (MSEI-Acute) (IQR 0-3) and 1.0 (MSEI-Chronic) (IQR 0-1). Ultrasound enthesitis was seen in 25 of 30 patients whereas clinical enthesitis was present in 15 patients only. USG picked up 20 (47 vs. 27) more sites of enthesitis as compared to clinical examination. The concordance rate was 89.4%. Discordance was more at tibial tuberosity, superior pole patella and tendoachilles entheses. Conclusions: Ultrasonography detects subclinical enthesitis in a proportion of patients with JIA-ERA. It can be a useful, cost-effective and safe diagnostic tool in the workup of JIA patients.
    No preview · Article · Jan 2016 · Clinical and experimental rheumatology