P23 Longitudinal antinuclear antibody (ANA) seroconversion in systemic lupus erythematosus: a prospective study of swedish cases with recent-onset disease

Background Immunoglobulin G (IgG) anti-nuclear antibodies (ANA) detected by indirect immunofluorescence (IF) microscopy remain a hallmark of systemic lupus erythematosus (SLE). Since it is controversial if IF-ANA status varies over time, we designed a prospective study with longitudinal follow-up of recent-onset patients with SLE. Methods The study population consisted of 54 newly diagnosed SLE cases, all meeting the 1982 ACR and/or the 2012 SLICC criteria. Clinical follow-up data, including disease activity and organ damage, and serum were collected from SLE onset and onwards, in most cases yearly (0 to 96 months). IF-ANA on HEp-2 cells was analysed and categorized regarding staining patterns. Using an addressable laser bead assay (ALBIA; FIDIS™ Connective profile), we measured IgG-ANA fine specificities to Ro52/SSA, Ro60/SSA, La/SSB, Sm, Sm/RNP, U1RNP, dsDNA, ribosomal P protein and histone. Results At baseline, all patients were judged IF-ANA positive at an abnormal titre corresponding to the 95th percentile of healthy blood donors, but seven of 54 patients (13%) lost IF-ANA-positivity over time, see figure 1. Homogenous (46%) and speckled (31%) were the most frequently observed staining patterns at inclusion, whereas 7% switched their pattern at least once during follow-up, see figure 1. Established associations between ANA fine-specificities and clinical data were confirmed. Levels of anti-Sm/RNP, but not of anti-dsDNA, correlated with clinical SLE disease activity (mSLEDAI-2K). Conclusion A considerable proportion of Swedish patients with SLE lose IF-ANA positivity over time. Consistent staining patterns were frequent. The clinical and mechanistic relevance of ANA seroconversion remains uncertain. Further prospective evaluations in larger SLE populations with diverse ethnicities are warranted. Acknowledgements We thank Marianne Petersson for biobank administration, all the clinicians for their efforts, and the staff at the Clinical Immunology laboratories in Linkoping and Uppsala. This work was supported by grants from the Swedish Rheumatism Association, the Region Ostergotland (ALF Grants), the Swedish Society of Medicine, the King Gustaf V’s 80-year Anniversary foundation and the King Gustaf V and Queen Victoria’s Freemasons foundation.