1,721,051 research outputs found
Prevention of seronegative rheumatoid arthritis: an entity of its own
No full textIn 1940, in his Oslo laboratory, Eric Waaler described rheumatoid factor—the first molecular marker identifying a subset of arthritis characterised by autoantibodies (ie, seropositive rheumatoid arthritis). This subset increased in size 60 years later with the discovery of anti-citrullinated protein antibody (ACPA). Instead of accepting that seropositive rheumatoid arthritis is different from seronegative rheumatoid arthritis, we stubbornly keep the unifying term rheumatoid arthritis, which mixes phenotypes that differ in origin, genetics, pathophysiology, and clinical course. With the TREAT EARLIER trial, Krijbolder and colleagues and Dumoulin and colleagues provide
further evidence that combining seropositive and seronegative rheumatoid arthritis into a single disease
might be a mistake
Seronegative rheumatoid arthritis: Neglected in clinical trials, a giant in clinical practice
No full textRheumatoid arthritis treatment : the earlier the better to prevent joint damage
Full text linkThe management of rheumatoid arthritis has undergone major advances in recent years, both in terms of the drugs armamentarium and therapeutic strategy. Treating disease to target, aiming at remission, through a tight control protocol is regarded as the standard of care. Reaching clinical and radiographic disease remission has therefore become an achievable goal. Increasing evidence has demonstrated that early diagnosis, prompt treatment initiation and early achievement of remission are the major predictors of long-term clinical, functional and radiographic outcomes. Concentrating efforts in controlling disease activity in a very early window of opportunity offers unique sustained benefits. In this short review, we analysed the available evidence supporting the value of treating rheumatoid arthritis early and the impact on disease outcomes, with particular focus on radiographic progression
Autoantibodies to heterogeneous nuclear ribonucleoproteins.
No full textThe aim of the present study was to investigate the effect of
long-term infliximab treatment on various autoantibodies in
patients with rheumatoid arthritis. Serum samples from 30
consecutive patients, who were prospectively followed during
infliximab and methotrexate therapy for refractory rheumatoid
arthritis, were tested at baseline and after 30, 54 and 78 weeks.
At these points, median values of the Disease Activity Score
were 6.38 (interquartile range 5.30–6.75), 3.69 (2.67–4.62),
2.9 (2.39–4.65) and 3.71 (2.62–5.06), respectively. Various
autoantibodies were assessed by standard indirect
immunofluorescence and/or ELISA. Initially, 50% of patients
were positive for antinuclear antibodies, and this figure
increased to 80% after 78 weeks (P = 0.029). A less marked,
similar increase was found for IgG and IgM anticardiolipin
antibody titre, whereas the frequency of anti-double-stranded
DNA antibodies (by ELISA) exhibited a transient rise (up to
16.7%) at 54 weeks and dropped to 0% at 78 weeks.
Antibodies to proteinase-3 and myeloperoxidase were not
detected. The proportion of patients who were positive for
rheumatoid factor (RF) was similar at baseline and at 78 weeks
(87% and 80%, respectively). However, the median RF titre
exhibited a progressive reduction from 128 IU/ml (interquartile
range 47–290 IU/ml) to 53 IU/ml (18–106 IU/ml). Anti-cyclic
citrullinated peptide (CCP) antibodies were found in 83% of
patients before therapy; anti-CCP antibody titre significantly
decreased at 30 weeks but returned to baseline thereafter. In
conclusion, the presence of anti-double-stranded DNA
antibodies is a transient phenomenon, despite a stable increase
in antinuclear and anticardiolipin antibodies. Also, the evolution
of RF titres and that of anti-CCP antibody titres differed during
long-term infliximab therapy
B cells in rheumatoid arthritis.
No full textThough its etiology remains unknown thus far, the role that autoimmune processes play in rheumatoid arthritis (RA) pathogenesis has been widely proven. Given the easier accessibility of humoral components, the first feature of this contribution to be recognized has been the occurrence of the so-called rheumatoid factor in a large proportion of RA patients. This antibody recognizes the Fc portion of human IgG. By investigating RA pathologic processes and also through experimental models where immune complexes play a fundamental role, many other autoantibodies have then come to our knowledge to be associated with the disease. Their presence and persistence implies that clones of autoreactive B cells survive and proliferate in RA patients under a continuous stimulation. Whether this is a mechanism of disease initiation or just an epiphenomenon is still unclear but no doubt exists that autoantibodies represent a very useful tool in both diagnostic and prognostic terms. Being much more than simple autoantibody producers, B cells are able to secrete many important cytokines and to efficiently present antigens to T lymphocytes in the synovial environment. All of these functions are essential in the development of RA, and lately have claimed attention as B cell depletion has become a common and effective strategy of treatment in RA
Dupilumab-induced enthesoarthritis and refractory atopic dermatitis successfully treated with baricitinib
No full textTreatment comparison in rheumatoid arthritis: Head-to-head trials and innovative study designs
Full text linkOver the last decades, the increasing knowledge in the area of rheumatoid arthritis has progressively expanded the arsenal of
available drugs, especially with the introduction of novel targeted therapies such as biological disease modifying antirheumatic
drugs (DMARDs). In this situation, rheumatologists are offered a wide range of treatment options, but on the other side the need
for comparisons between available drugs becomes more and more crucial in order to better define the strategies for the choice and
the optimal sequencing. Indirect comparisons ormeta-analyses of data coming fromdifferent randomised controlled trials (RCTs)
are not immune to conceptual and technical challenges and often provide inconsistent results. In this review we examine some
of the possible evolutions of traditional RCTs, such as the inclusion of active comparators, aimed at individualising treatments in
real-life conditions. Although head-to-head RCTs may be considered the best tool to directly compare the efficacy and safety of two
different DMARDs, surprisingly only 20 studies with such design have been published in the last 25 years. Given the recent advent
of the first RCTs truly comparing biological DMARDs, we also review the state of the art of head-to-head trials in RA
Assessment of synovitis to predict bone erosions in rheumatoid arthritis
No full textAlthough rheumatoid arthritis (RA) is traditionally considered as the prototype of destructive arthritis, the course of the disease varies considerably, with some patients experiencing more rapid progression of joint damage and disability than others. Given the increasing availability of treatment targets and options, timely recognition of individual's outcomes could allow therapeutic allocation according to personalized benefit-risk profiles. Research efforts are thus increasingly focused at discovering predictive markers that could identify patients with aggressive, rapidly progressive disease and poor prognosis. As joint destruction in RA is the result of the cumulative burden of inflammation, variables reflecting the severity of synovitis and its persistence over time might refine our ability to build early prognostic algorithms. The goal of this article is to review the clinical implications of the assessment of synovitis in relation to radiographic outcomes. Traditional and novel assessment tools will be discussed, including clinical measures, imaging techniques and tissue biomarkers. Achievements in the field of synovial tissue analysis and peripheral blood biomarkers of synovitis represent only the first steps of ongoing progress, which still need to be integrated into the phenotypic heterogeneity of RA
What can we learn from treatment-induced changes in rheumatoid factor and anti-citrullinated peptide antibodies?
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