053. Reasons for Treatment Delay in Early Rheumatoid Arthritis Differ According to Autoantibody Status

Background: Evidence for a 12 week window of opportunity after symptom onset, during which therapeutic intervention meaningfully interrupts the natural history of RA, has led to a proliferation of early arthritis clinics (EACs) intended to expedite diagnosis. However, patients continue to experience delays between symptom onset and treatment initiation. Optimal interventions for improving access to DMARD therapy may differ between sub-groups of patients with RA. Methods: A single-centre retrospective analysis of a UK early RA inception cohort was undertaken to identify those components of the overall time-delay between symptom onset and treatment initiation that differed according to patients’ autoantibody status. The primary time periods examined were symptom onset to Rheumatology referral, Rheumatology referral to EAC appointment and EAC appointment to DMARD initiation. For a subgroup of patients sufficient data was available to divide the first period into two parts: symptom onset to first general practitioner (GP) visit and first GP visit to Rheumatology referral. Detailed baseline characteristics were recorded, including serological status for RF and ACPAs. Time periods were dichotomized and data were analysed using Pearson’s chi-squared test (with Wald’s continuity correction for 2 (cid:2) 2 contingencies), with a ¼ 5%. Results: 166 RA patients were diagnosed over a 31 month period, of whom 78 (47%) were ACPA/RF double seropositive, 54 (33%) double-seronegative, and 15 (9%) ACPA and 19 (11%) RF single seropositive, respectively. Overall, the time between symptom onset and DMARD initiation was similar between all serotypes (median 16 weeks). Compared with their seropositive counterparts, double-seronegative to experience delays between presentation in secondary care and DMARD initiation ( P < 0.05), whereas ACPA-positive patients were more likely to experience delays of > 12 weeks between symptom onset and referral from primary to care ( P < 0.05). Among a subgroup of 32 RA patients in whom data were available, this delay in presentation of ACPA-positive patients to secondary care was accounted for by a prolonged symptom duration prior to first consultation in primary care ( P < 0.05) – and not by delayed referral. Conclusion: Our exploratory analysis has identified the potential for bottlenecks in the diagnosis and treatment of RA to differ in their contribution to treatment delays according to patients’ autoantibody status. In particular, our findings add credence to previous hints that seropositivity predicts a patient’s tendency to defer seeking medical advice for joint pain. The observation warrants large-scale validation and, if confirmed, awaits mechanistic explanation. Our findings also highlight that the ongoing clinical challenge of diagnosing seronegative RA may account for delayed access to treatment in this group. An improved understanding of these factors should inform the design of service delivery for early arthritis patients in the future. Disclosure statement: The authors have declared no conflicts of interest.