Competencies in rheumatology: a European framework

The aims, structure, methods and educational experiences employed in the training of rheumatologists vary from one national programme to another, according to traditions, rules and resources. Mutual recognition of titles, the free movement of labour and the striving towards for high-quality standards in medical care in Europe demand that efforts and progress are made to ensure that similar competencies are achieved by different programmes. The European Rheumatology Curriculum Framework, developed by the European Board of Rheumatology, is meant to be a step towards the harmonization of rheumatology specialist training within the European Union, by providing a reference framework to the development and benchmarking of national curricula for the specialist training of rheumatologists. The European Rheumatology Curriculum Framework has now been endorsed by scientific and educational bodies in 17 member countries. It has been provided with a contextualized review of good practice in curriculum planning and development - the European Board of Rheumatology Educational Guide

Autoantibody Epitope Spreading in the Pre-Clinical Phase Predicts Progression to Rheumatoid Arthritis

Rheumatoid arthritis (RA) is a prototypical autoimmune arthritis affecting nearly 1% of the world population and is a significant cause of worldwide disability. Though prior studies have demonstrated the appearance of RA-related autoantibodies years before the onset of clinical RA, the pattern of immunologic events preceding the development of RA remains unclear. To characterize the evolution of the autoantibody response in the preclinical phase of RA, we used a novel multiplex autoantigen array to evaluate development of the anti-citrullinated protein antibodies (ACPA) and to determine if epitope spread correlates with rise in serum cytokines and imminent onset of clinical RA. To do so, we utilized a cohort of 81 patients with clinical RA for whom stored serum was available from 1–12 years prior to disease onset. We evaluated the accumulation of ACPA subtypes over time and correlated this accumulation with elevations in serum cytokines. We then used logistic regression to identify a profile of biomarkers which predicts the imminent onset of clinical RA (defined as within 2 years of testing). We observed a time-dependent expansion of ACPA specificity with the number of ACPA subtypes. At the earliest timepoints, we found autoantibodies targeting several innate immune ligands including citrullinated histones, fibrinogen, and biglycan, thus providing insights into the earliest autoantigen targets and potential mechanisms underlying the onset and development of autoimmunity in RA. Additionally, expansion of the ACPA response strongly predicted elevations in many inflammatory cytokines including TNF-α, IL-6, IL-12p70, and IFN-γ. Thus, we observe that the preclinical phase of RA is characterized by an accumulation of multiple autoantibody specificities reflecting the process of epitope spread. Epitope expansion is closely correlated with the appearance of preclinical inflammation, and we identify a biomarker profile including autoantibodies and cytokines which predicts the imminent onset of clinical arthritis