LAUSR

Background: Despite recent progress in biomarker discovery for RA diagnostics, still over one third of RA patients are seronegative for RF and ACPA, a number which is even higher in early disease. In both the University of Hasselt (UH) cohort (n=292) and Leiden Early Arthritis Clinic (EAC) cohort (n=600), 38% of RA patients were seronegative for RF and ACPA. Testing for novel autoantibodies to UH peptides UH-RA.1 and UH-RA.21, reduced the serological gap from 38% to 29% in the UH cohort (P=0.03) and from 38% to 32% in the EAC cohort (P=0.01), with associated specificities in rheumatic controls ranging from 88–96% 1. Objectives: Our aim is to validate the reactivities of autoantibodies against UH-RA.1 and UH-RA.21 peptides in early and seronegative RA patients from the CareRA cohort. Methods: Peptide enzyme-linked immunosorbent assays have been developed to screen for the presence of antibodies to UH-RA peptides. Cut-off for seropositivity was defined by 2 x SD above the mean antibody level of the healthy control group 1. Antibody reactivity to UH-RA.1 and UH-RA.21 was evaluated in baseline samples, collected before the start of treatment, of 223 early RA patients from the CareRA cohort. Results: Antibodies to UH-RA.1 and UH-RA.21 were found in respectively 5% and 21% of the baseline samples from the CareRA cohort. These antibodies were found in similar levels in both RF/ACPA seropositive and seronegative patients. In the CareRA cohort, 24% of patients were seronegative for RF and ACPA and combining the presence of autoantibodies to UH-RA.1 and UH-RA.21 with RF/ACPA serology, reduced the seronegative population from 24 % to 18% (P=0.13). Conclusions: Screening for antibodies against novel UH peptides UH-RA.1 and UH-RA.21 has now been performed in three large independent cohorts. This study validates the presence of antibody reactivity to these UH-RA peptides in seronegative and early RA. This might reinforce current diagnostics and improve early diagnosis and intervention in RA. Reference 1. De Winter, et al. Rheumatology (Oxford)2016;55(8):1431–6. Disclosure of Interest: None declared