Recommendation For numbered afﬁliations see end of article Correspondence to Danielle M Gerlag, Division of Clinical Immunology and Rheumatology, Academic Medical Center/University of Amsterdam, F4-105 PO Box 22700, 1100 DE Amsterdam, The Netherlands; d.m.gerlag@amc.uva.nl Handling editor Johannes WJ Bijlsma Received 1 November 2011 Accepted 23 January 2012 Published Online First 2 March 2012 EULAR recommendations for terminology and research in individuals at risk of rheumatoid arthritis: report from the Study Group for Risk Factors for Rheumatoid Arthritis Danielle M Gerlag,1 Karim Raza,2 Lisa G M van Baarsen,1 Elisabeth Brouwer,3 Christopher D Buckley,2 Gerd R Burmester,4 Cem Gabay,5 Anca I Catrina,6 Andrew P Cope,7 François Cornelis,8 Solbritt Rantapää Dahlqvist,9 Paul Emery,10 Stephen Eyre,11 Axel Finckh,5 Steffen Gay,12 Johanna M Hazes,13 Annette van der Helm-van Mil,14 Tom W J Huizinga,14 Lars Klareskog,6 Tore K Kvien,15 Cathryn Lewis,7 Klaus P Machold,16 Johan Rönnelid,17 Dirkjan van Schaardenburg,18 Georg Schett,19 Josef S Smolen,16 Sue Thomas,20 Jane Worthington,11 Paul P Tak1 ABSTRACT The Study Group for Risk Factors for Rheumatoid Arthritis was established by the EULAR Standing Committee on Investigative Rheumatology to facilitate research into the preclinical and earliest clinically apparent phases of rheumatoid arthritis (RA). This report describes the recommendation for terminology to be used to deﬁne speciﬁc subgroups during different phases of disease, and deﬁnes the priorities for research in this area. Terminology was discussed by way of a three-stage structured process: A provisional list of descriptors for each of the possible phases preceding the diagnosis of RA were circulated to members of the study group for review and feedback. Anonymised comments from the members on this list were fed back to participants before a 2-day meeting. 18 participants met to discuss these data, agree terminologies and prioritise important research questions. The study group recommended that, in prospective studies, individuals without RA are described as having: genetic risk factors for RA; environmental risk factors for RA; systemic autoimmunity associated with RA; symptoms without clinical arthritis; unclassiﬁed arthritis; which may be used in a combinatorial manner. It was recommended that the preﬁx ‘pre-RA with:’ could be used before any/any combination of the ﬁve points above but only to describe retrospectively a phase that an individual had progressed through once it was known that they have developed RA. An approach to dating disease onset was recommended. In addition, important areas for research were proposed, including research of other tissues in which an adaptive immune response may be initiated, and the identiﬁcation of additional risk factors and biomarkers for the development of RA, its progression and the development of extra- articular features. These recommendations provide guidance on approaches to describe phases before the development of RA that will facilitate communication between researchers and comparisons between studies. A number of research questions have been deﬁned, requiring new cohorts to be established and new techniques to be developed to image and collect material from different sites. Rheumatoid arthritis (RA) is a prototype immune- mediated inﬂammatory disease, characterised by a symmetric polyarthritis usually involving the small joints of the hands and feet. Other joints can also be involved. Rheumatoid factor (RF) and/or anticitrullinated protein antibody (ACPA) positive (‘seropositive’) RA is associated with more aggres- sive articular disease, a higher frequency of extra- articular manifestations and increased mortality.1 RA is still associated with signiﬁcant morbidity despite major developments in antirheumatic ther- apy. Among the inﬂammatory joint diseases, RA is the commonest and the most important in socio- economic terms. Over the past few years, research in the ﬁeld of RA has focused on the earliest stages of disease, leading to the discovery that circulating autoan- tibodies, speciﬁcally immunoglobulin M-RF and ACPA, and increased acute phase reactants precede the clinical onset of the disease.2–5 These autoanti- bodies are present a median of 5 years before clini- cal symptoms appear.3 Subjects with arthralgia and these autoantibodies have an approximately 30% chance of developing RA within 1 year.6 These data form strong evidence that clinical signs and symptoms may be preceded by a preclinical phase for several years, and that the preclinical and ear- liest clinically apparent phases of RA are likely to represent important therapeutic windows within which clinical outcomes can be dramatically modu- lated.7 Factors such as smoking, which act during the preclinical phase, leading to citrullination of peptides and ACPA formation,8 are increasingly being recognised. To facilitate research in this area, the European League Against Rheumatism (EULAR) Standing Committee on Investigative Rheumatology estab- lished a study group in February 2011 to build a European network of excellence. Key aims of this study group were to develop a more accu- rate understanding of the mechanisms driving the immunological abnormalities seen during the preclinical phase of RA and the stimuli that turn such abnormalities into a joint-centric disease, in 638 Ann Rheum Dis 2012;71:638–641. doi:10.1136/annrheumdis-2011-200990