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Arthritis Research & Therapy - Latest Articles

Automated evaluation of autoantibodies on human epithelial-2 cells as an approach to standardize cell-based immunofluorescence tests
Karl EgererDirk RoggenbuckRico HiemannMax-Georg WeyerThomas BuettnerBoris RadauRosemarie KrauseBarbara LehmannEugen FeistGerd-Rudiger Burmester Tue, 09 Mar 2010 00:00:00 -0000
IntroductionAnalysis of autoantibodies (AAB) by indirect immunofluorescence (IIF) is a basic tool for the serological diagnosis of systemic rheumatic disorders. Automation of AAB IIF reading including pattern recognition may improve intra- and inter-laboratory variability and meet the demand for cost-effective assessment of large numbers of samples. Comparing automated and visual interpretation, the usefulness for routine laboratory diagnostics was investigated. Methods: Autoantibody detection by IIF on human epithelial-2 (HEp-2) cells was conducted in a total of 1222 consecutive sera of patients with suspected systemic rheumatic diseases from a university routine laboratory (n=924) and a private referral laboratory (n=298). IIF results from routine diagnostics were compared with a novel automated interpretation system. Results: Both diagnostic procedures showed a very good agreement in detecting AAB (kappa=0.828) and differentiating respective immunofluorescence patterns. Only 98 (8.0%) of 1222 sera demonstrated discrepant results in the differentiation of positive from negative samples. The contingency coefficient of Chi-square statistics was 0.646 for the university laboratory cohort with an agreement of 93.0% and 0.695 for the private laboratory cohort with an agreement of 90.6%, P<0.0001, respectively. Comparing immunofluorescence patterns, 111 (15.3%) sera yielded differing results. Conclusions: Automated assessment of AAB by IIF on HEp-2 cells using an automated interpretation system is a reliable and robust method for positive/negative differentiation. Employing novel mathematical algorithms, automated interpretation provides reproducible detection of specific immunofluorescence patterns on HEp-2 cells. Automated interpretation can reduce drawbacks of IIF for AAB detection in routine diagnostics providing more reliable data for clinicians.
Circulating surfactant protein -D is low and correlates negatively with systemic inflammation in early, untreated rheumatoid arthritis
Anne ChristensenGrith SorensenKim Horslev-PetersenUffe HolmskovHanne LindegaardKirsten JunkerMerete HetlandKristian Stengaard-PedersenSoren JacobsenTine LottenburgerTorkell EllingsenLis AndersenIb HansenHenrik SkjodtJens PedersenUlrik LauridsenAnders SvendsenUlrik TarpJan PodenphantAage VestergaardAnne Grethe JurikMikkel OstergaardPeter Junker Mon, 08 Mar 2010 00:00:00 -0000
IntroductionSurfactant protein D (SP-D) is a collectin with immuno-regulatory functions, which may depend on oligomerization. Anti-microbial and anti-inflammatory properties have been attributed to multimeric SP-D variants, while trimeric subunits per se have been suggested to enhance inflammation. Previously, we reported low circulating SP-D in early rheumatoid arthritis (RA), and the present investigation aims to extend these data by serial SP-D serum measurements, studies on synovial fluid, SP-D size distribution and genotyping in patients with early RA. Methods: One-hundred-and-sixty DMARD naive RA patients with disease duration less than 6 months were studied prospectively for 4 years (CIMESTRA trial) including disease activity measures (C-reactive protein, joint counts and Health Assessment Questionnaire (HAQ) score), autoantibodies, x-ray findings and SP-D. SP-D was quantified by enzyme-linked immunosorbent assay (ELISA) and molecular size distribution was assessed by gel filtration chromatography. Further, SP-D Met11Thr single nucleotide polymorphism (SNP) analysis was performed. Results: Serum SP-D was significantly lower in RA patients at baseline compared with healthy controls (p<0.001). SP-D increased slightly during follow-up (p<0.001), but was still subnormal at 4 years after adjustment for confounders (p<0.001). SP-D in synovial fluid was up to 2.5-fold lower than in serum. While multimeric variants were detected in serum, SP-D in synovial fluid comprised trimeric subunits only. There were no significant associations between genotype distribution and SP-D. Baseline SP-D was inversely associated to CRP and HAQ score. A similar relationship was observed regarding temporal changes in SP-D and CRP (0-4 years). SP-D was not associated to x-ray findings. Conclusions: This study confirms that circulating SP-D is persistently subnormal in early and untreated RA despite a favourable therapeutic response obtained during 4-years follow-up. SP-D correlated negatively to disease activity measures, but was not correlated with x-ray progression or SP-D genotype. These observations suggest that SP-D is implicated in RA pathogenesis at the protein level. The exclusive presence of trimeric SP-D in affected joints may contribute to the maintenance of joint inflammation.Trial registration (j.nr NCT00209859).
TRAF1/C5 polymorphism is not associated with increased mortality in rheumatoid arthritis; two large longitudinal studies
Jessica van NiesRute MarquesStella TrompetZuzana de JongFina KurreemanRene ToesJ.Wouter JukemaTom HuizingaAnnette van der Helm-van Mil Fri, 05 Mar 2010 00:00:00 -0000
IntroductionRecently an association between a genetic variation in TRAF1/C5 and mortality from sepsis or cancer was found in rheumatoid arthritis (RA). The most prevalent cause of death, cardiovascular disease, may have been missed in that study, since patients were enrolled at an advanced disease stage. Therefore, we used an inception cohort of RA patients to investigate the association between TRAF1/C5 and cardiovascular mortality, and replicate the findings on all-cause mortality. As TRAF1/C5 associated mortality may not be restricted to RA, we also studied a large cohort of non-RA patients. Methods: 615 RA patients from the Leiden Early Arthritis Clinic (EAC) (mean follow-up 7.6 years) were genotyped for rs10818488. In addition 5634 persons enrolled in the PROspective Study of Pravastatin in the Elderly at Risk (mean follow-up 3.2 years) were genotyped for rs2416808 (R2 >0.99 with rs10818488). The life/death status was determined and for the deceased persons the cause of death was ascertained. Cox proportional hazards and regression models were used to assess hazard ratios (HR) and 95% confidence intervals (CI). Results: Seventy-seven RA patients died. The main death causes in RA patients were cardiovascular diseases (37.7%), cancer (28.6%) and death due to infections (9.1%). No association was observed between the rs10818488 susceptible genotype AA and cardiovascular mortality (HR 1.08 95%CI 0.54 to 2.15) and all-cause mortality (HR 0.81 95%CI 0.27 to 2.43). Similar findings were observed for rs2416808 susceptible genotype GG in the non-RA cohort (HR 0.99; 95%CI 0.79 to 1.25 and HR 0.89; 95%CI 0.64 to 1.25, respectively). Conclusions: The TRAF1/C5 region is not associated with an increased mortality risk.
Urokinase-type plasminogen activator and arthritis progression: role in systemic disease with immune complex involvement
Andrew CookChristine De NardoEmma BraineAmanda TurnerRoss VlahosKerrie WayS Kaye BeckmanJason LenzoJohn Hamilton Tue, 02 Mar 2010 00:00:00 -0000
IntroductionUrokinase-type plasminogen activator (u-PA) has been implicated in fibrinolysis, cell migration, latent cytokine activation, cell activation, T cell activation, and tissue remodeling, all of which are involved in the development of rheumatoid arthritis. Previously, u-PA has been reported to play a protective role in monoarticular arthritis models involving mBSA as the antigen, but a deleterious role in the systemic polyarticular collagen-induced arthritis (CIA) model. The Aim of the current study is to determine how u-PA might be acting in systemic arthritis models. Methods: The CIA model and bone marrow chimeras were used to determine the cellular source of u-PA required for the arthritis development. Gene expression of inflammatory and destructive mediators was measured in joint tissue by quantitiative PCR and protein levels by ELISA. The requirement for u-PA in the type II collagen (CII)-mAb induced arthritis (CAIA) and K/BxN serum transfer arthritis models was determined using u-PA-/- mice. Neutrophilia was induced in the peritoneal cavity using either ovalbumin/anti-ovalbumin, or the complement component C5a. Results: u-PA from a bone marrow-derived cell was required for the full development of CIA. The disease in u-PA-/- mice reconstituted with bone marrrow from C57BL/6 mice was indistinguishable from that in C57BL/6 mice, in terms of clincal score, histologic features, and protein and gene expression of key mediators. u-PA-/- mice were resistant to both CAIA and K/BxN serum transfer arthritis development. u-PA-/- mice developed a reduced neutrophilia and chemokine production in the peritoneal cavity following OVA/anti-OVA injection; in contrast, the peritoneal neutrophilia in response to C5a was u-PA independent. Conclusions: u-PA is required for the full development of systemic arthritis models involving immune complex formation and deposition. The cellular source of u-PA required for CIA is bone marrow-derived and likely to be of myeloid origin. For immune complex-mediated peritonitis, and perhaps some other inflammatory responses, it is suggested that the u-PA involvement may be upstream of C5a signaling.
Diagnostic value of anti-cyclic citrullinated peptides and association with HLA-DRB1 shared epitope alleles in African rheumatoid arthritis patients
Madeleine Singwe-NgandeuAxel FinckhSylvette BasJean-Marie TiercyCem Gabay Tue, 02 Mar 2010 00:00:00 -0000
IntroductionTo examine the diagnostic performance of autoantibodies against citrullinated peptides/proteins (ACPA) and to determine the prevalence of HLA-DRB1 shared epitope alleles (SE) in African patients with rheumatoid arthritis (RA). Methods: Serum levels of anti-cyclic citrullinated peptides antibodies (anti-CCP2, anti-CCP3), IgM and IgA rheumatoid factors (RF) were measured by enzyme-linked immunosorbent assay in the serum of 56 consecutive RA patients regularly followed in the Rheumatology Unit of Yaounde, Cameroon. Genotyping of HLA-DRB1 alleles was performed by polymerase chain reaction and hybridization with sequence-specific oligonucleotide probes on microbeads arrays. 51 patients with other inflammatory rheumatic diseases and 50 healthy individuals were included as controls. Results: Anti-CCP2 assay showed the best diagnosis sensitivity (82%) and specificity (98%) with high PPV (96%) and NPV (91%). 30% of RA patients were bearing at least one copy of the HLA-DRB1 shared epitope (SE) compared to 10% and 14% of patients with other inflammatory rheumatic diseases and healthy individuals, respectively. The presence of the SE was associated with the production of ACPA. Conclusions: Anti-CCP2 antibodies are useful markers of RA in African patients. In this cohort, the prevalence of the SE is higher in RA patients than in controls but lower than that reported in patients cohorts of European ancestry. The discrepancy between the high prevalence of ACPA-positive patients and the relatively low number of SE-positive cases suggest that, in addition to SE, other genetic factors control the development of ACPA in African RA patients.
The loss of health status in rheumatoid arthritis and the effect of biologic therapy: a longitudinal observational study
Frederick WolfeKaleb Michaud Tue, 02 Mar 2010 00:00:00 -0000
IntroductionThe long-term course of rheumatoid arthritis (RA) in terms of health status is not well understood, nor is the degree of effectiveness of biologic therapy in the community. We modeled the progression of loss of health status, and measured incremental costs and effectiveness of biologic therapy in the community. Methods: We studied change in function and health status in 18,485 RA patients (135,731 observations) at 6-month intervals for up to 11 years, including a group of 4,911 patients (59,630 observations) who switched to biologic therapy from non-biologic therapy. We measured the SF-36 Physical Component (PCS) and Mental Component (MCS) Summary scales, the EQ-5D health utility scale, and the Health Assessment Questionnaire (HAQ) disability scale; and we calculated treatment and direct medical costs. Results: RA onset caused an immediate and substantial reduction in physical but not mental health status. Thereafter, the progression of dysfunction in RA was very slow (HAQ 0.016 units and PCS -0.125 units annually), only slightly worse than the age and sex-adjusted US population. We estimated biologic treatment to improve HAQ by 0.29 units, PCS by 5.3 units, and EQ-5D by 0.05 units over a 10-year period. The estimated incremental 10-year total direct medical cost for this benefit was $159,140. Conclusions: Biologic therapy retards RA progression, but its effect is far less than is seen in clinical trials. In the community, cost-effectiveness is substantially less than that estimated from clinical trial data. The study results represent the incremental benefit of adding biologic therapy to optimum non-biologic therapy.

Annals of the Rheumatic Diseases current issue

Rheumatoid arthritis and pregnancy; not only for rheumatologists interested in female health issues
Dolhain, R. J E M
Anti-endothelial cell antibodies in systemic sclerosis
Mihai, C, Tervaert, J W C Anti-endothelial cell antibodies (AECA) are a heterogeneous class of antibodies whose role in the pathogenesis of autoimmune diseases with vascular involvement has been extensively studied. Systemic sclerosis (SSc) is one of the systemic autoimmune diseases in which endothelial dysfunction is well defined and important in the development of the disease. AECA are present in the serum samples of many patients with SSc. Depending on the detection method and on patient selection, 22–86% of patients test positive for AECA. Among the demonstrated clinical associations, lung and peripheral vascular involvement are the most common. In this paper, the methods of detection, various molecular specificities and the possible pathogenic mechanisms of AECA in SSc are reviewed.
EULAR evidence-based recommendations for cardiovascular risk management in patients with rheumatoid arthritis and other forms of inflammatory arthritis
Peters, M J L, Symmons, D P M, McCarey, D, Dijkmans, B A C, Nicola, P, Kvien, T K, McInnes, I B, Haentzschel, H, Gonzalez-Gay, M A, Provan, S, Semb, A, Sidiropoulos, P, Kitas, G, Smulders, Y M, Soubrier, M, Szekanecz, Z, Sattar, N, Nurmohamed, M T Objectives: To develop evidence-based EULAR recommendations for cardiovascular (CV) risk management in patients with rheumatoid arthritis (RA), ankylosing spondylitis (AS) and psoriatic arthritis (PsA). Methods: A multidisciplinary expert committee was convened as a task force of the EULAR Standing Committee for Clinical Affairs (ESCCA), comprising 18 members including rheumatologists, cardiologists, internists and epidemiologists, representing nine European countries. Problem areas and related keywords for systematic literature research were identified. A systematic literature research was performed using MedLine, Embase and the Cochrane library through to May 2008. Based on this literature review and in accordance with the EULAR’s "standardised operating procedures", the multidisciplinary steering committee formulated evidence-based and expert opinion-based recommendations for CV risk screening and management in patients with inflammatory arthritis. Results: Annual CV risk assessment using national guidelines is recommended for all patients with RA and should be considered for all patients with AS and PsA. Any CV risk factors identified should be managed according to local guidelines. If no local guidelines are available, CV risk management should be carried out according to the SCORE function. In addition to appropriate CV risk management, aggressive suppression of the inflammatory process is recommended to further lower the CV risk. Conclusions: Ten recommendations were made for CV risk management in patients with RA, AS and PsA. The strength of the recommendations differed between RA on the one hand, and AS and PsA, on the other, as evidence for an increased CV risk is most compelling for RA.
Postpartum onset of rheumatoid arthritis and other chronic arthritides: results from a patient register linked to a medical birth registry
Wallenius, M, Skomsvoll, J F, Irgens, L M, Salvesen, K A, Koldingsnes, W, Mikkelsen, K, Kaufmann, C, Kvien, T K Background: It is known that onset of rheumatoid arthritis (RA) is increased post partum. Objective: To compare incidence rates between RA and other chronic arthritides (OCA) 0–24 months after delivery, and to compare the incidence rates within each group 0–24 versus 25–48 months post partum. Methods: Premenopausal women from a Norwegian patient register were linked with the Medical Birth Registry of Norway to study the interval between delivery and time of diagnosis. Cox regression analysis with adjustments for age at delivery and birth order was applied to compare proportions of incident cases of RA and OCA with onset 0–24 months post partum. Poisson regression analysis with adjustment for the population at risk was applied to estimate the incidence rate ratio (IRR) 0–24 versus 25–48 months post partum. Results: Of 183 RA and 110 patients with OCA diagnosed after delivery, 69 (37.7%) had RA and 31 (28.2%) OCA during the first 24 months post partum (p = 0.09). The IRR (95% CI) for diagnosis during 0–24 months versus 25–48 months was 1.73 (1.11 to 2.70) (p = 0.01) for RA, 1.05 (0.59 to 1.84) (p = 0.86) for OCA. The IRR was 2.23 (1.06 to 4.70) and 1.87 (0.67 to 5.21), respectively, when only considering diagnoses after the first pregnancy. Clinical characteristics were similar within each diagnostic group. Conclusion: The proportions of incident cases with onset 0–24 months after delivery were not different between RA and OCA. A peak in incidence during 0–24 months was seen in the RA group, both when considering all pregnancies and only the first pregnancy.
Correction

Does anti-mutated citrullinated vimentin have additional value as a serological marker in the diagnostic and prognostic investigation of patients with rheumatoid arthritis? A systematic review
Luime, J J, Colin, E M, Hazes, J M W, Lubberts, E Objective: To review the diagnostic and prognostic value of anti-mutated citrullinated vimentin (MCV) in rheumatoid arthritis, taking into account the already available serology. Methods: Medline was searched via PubMed (1966 to May 2008) for anti-MCV and related terms, arthritis and arthropathies. Studies with anti-MCV, arthritis/arthropathy, and primary data on diagnosis and/or prognosis were included. Their methodological quality was assessed using the Quality Assessment of Diagnostic Accuracy Studies (QUADAS) instrument for diagnostic studies and the modified Hayden list for prognostic studies. Results: Of 14 eligible studies, 11 included diagnostic data and 3 included prognostic data. No study evaluated anti-MCV as an added diagnostic test to the already available anti-cyclic citrullinated peptide (CCP) and rheumatoid factor serology. One study included the optimal patient spectrum resulting in a sensitivity of 0.59 and specificity of 0.98. A total of 10 diagnostic case-control studies using the same anti-MCV kit showed a sensitivity of 0.64–0.84 and a specificity of 0.79–0.96. This almost equalled the performance of anti-CCP in the same studies. The prognostic evaluation of anti-MCV was limited by differences in study methodology, outcome and statistical modelling. Individual studies showed moderate associations for anti-MCV and radiological progression with the strength of the association comparable to that of anti-CCP. Conclusions: Study heterogeneity, choice of study population and methodological limitations limited overall conclusions about the true diagnostic and prognostic test performance of anti-MCV. Evidence from the diagnostic case-control studies suggests that anti-MCV may be used as an alternative for anti-CCP.

Arthritis Care & Research

The child, grown, becomes independent
Patricia P. Katz, Edward H. Yelin, Michael D. Lockshin Mon, 30 Nov 2009 12:54:00 -0000
No abstract.
Getting them even earlier: Identifying individuals before clinical presentation with rheumatoid arthritis
Katherine P. Liao, Karen H. Costenbader Mon, 30 Nov 2009 12:54:00 -0000
No abstract.
Each measure of patient-reported change provides useful information and is susceptible to bias: The need to combine methods to assess their relative validity
Pythia T. Nieuwkerk, Mirjam A. G. Sprangers Mon, 30 Nov 2009 12:54:00 -0000
No abstract.

Arthritis & Rheumatism

In this issue
Thu, 25 Feb 2010 15:39:00 -0000
No abstract.
Should antibodies to high-density lipoprotein cholesterol and its components be measured in all systemic lupus erythematosus patients to predict risk of atherosclerosis?
Bevra H. Hahn Thu, 07 Jan 2010 12:22:00 -0000
No abstract.
The synovial lining micromass system: Toward rheumatoid arthritis in a dish?
Harris Perlman, Richard M. Pope Thu, 25 Feb 2010 15:39:00 -0000
No abstract.

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