Ab0897 the presence of anti-u1-rnp antibody has a mild but apparent impact on interstitial lung disease in patients with systemic sclerosis

Background Interstitial lung disease (ILD) is the leading cause of systemic sclerosis (SSc)-related death[1]. With the availability of antifibrotic agents to slow the progression of SSc-ILD[2], it is important for clinicians to be aware of the antibody profile predicting the severity and progression of SSc-ILD. Objectives To determine the impact of anti-U1 ribonucleoprotein antibody (αRNPab) in addition to anti-topoisomerase 1 antibody (ATA) on SSc related interstitial lung disease (ILD). Methods Patients with SSc who visited Mie University Hospital between December 2020 to December 2021 were consecutively registered. The severity and progression of ILD on chest computed tomography (CT) were assessed based on the ILD and traction bronchiectasis (TBE) scores, evaluated by using established method [3] with minor modification. We hypothesized that ATA had the greatest impact on ILD, followed by αRNPab, and accordingly stratified patients into three groups: group 1, ATA-positive; group 2, αRNPab-positive; and group 3, double-negative. At registration, patient characteristics were compared according to the presence of ILD, and the severity of ILD were compared among three groups. For patients who had earlier CT scans available, ILD progression was assessed. Results Among 48 patients (ILD/non-ILD; n=25/23), αRNPab positivity was significantly higher in the ILD than in the non-ILD group (32%, 0%, p<0.01). In 47 patients, the percentage of patients whose ILD score ≥ 20% was 83.3, 28.5 and 5.8% in groups 1, 2 and 3 (n = 6/7/34), respectively (p<0.01). In 25 patients, the percentage of patients with progressive ILD whose ILD score increased by ≥ 5% was 80.0, 50.0 and 14.3% in groups 1, 2 and 3 (n = 5/6/14), respectively (p<0.01). Conclusion The presence of αRNPab significantly affects the presence, severity and progression of SSc-ILD, although the effect is milder than that of ATA. References [1]Khanna D, et al. Arthritis Rheumatol 2022;74(1):13-27. [2]Distler O, et al. N Engl J Med 2019;380(26):2518-28. [3]Walsh SL, et al. Thorax 2014;69(3):216-22. Acknowledgements I have no acknowledThis work was supported by Nippon Boehringer Ingelheim Co., Ltd., Chugai Pharmaceutical Co., Ltd. and Mitsubishi Tanabe Pharma Corporation and AbbVie GK for the cost of anti-ARS antibody measurement. The design, execution, and interpretation of results for this study were entirely independent of these companies.gements to declare. Disclosure of Interests None Declared.