THU0343 AUTOANTIBODIES CAN PARTLY PREDICT SEVERITY OF DAMAGE BUT NOT EXTENT IN PATIENTS WITH IDIOPATHIC INFLAMMATORY MYOSITIS
Authors: F. Espinosa-Ortega, M. Holmqvist, M. Dastmalchi, A. Mammen, I. E. Lundberg, H. Alexanderson
Journal: Annals of the Rheumatic Diseases (2020)

Background: Patients with idiopathic inflammatory myopathies (IIM) might suffer from irreversible damage once inflammation has decreased. Autoantibodies are found in up to 80% of patients with IIM and are coupled with specific clinical features. Whether autoantibodies can be used as biomarkers to predict patterns of damage in IIM remains unknown. Objectives: To investigate the association between autoantibodies and organ damage in patients with IIM using longitudinal national register data. Methods: Data were retrieved from the electronic Swedish Rheumatology Quality Register (SRQ). Patients (n=302) with a clinical diagnosis of IIM (2017 EULAR/ACR criteria) were included. Autoantibody status was tested by either line blot or RNA- and protein immunoprecipitation; HMGCR and FHL-1 autoantibodies were tested by ELISA. Patients were grouped into six categories of autoantibodies (Table 1). The Myositis Damage Index (MDI) score was applied to measure organ damage using both components ( extent and severity ) as a continuous variable and were analyzed using generalized estimating equations (GEE). A categorical variable for each time point of MDI assessment since diagnosis was created to adjust for time (Table 2). A base model which included autoantibody group and time was fit. Other potential predictors included age at diagnosis, sex, disease duration from diagnosis to inclusion to SRQ, arthritis, Raynaud, mechanics’ hands and heart involvement at registry; core set measures at each MDI time point allowing multiple longitudinal observations were also tested. Table 1. Clinical diagnosis and autoantibody groups. Diagnosis N (%) Polymyositis 119 (38) Dermatomyositis (DM) 99 (33) Inclusion body myositis 35 (12) Amyopathic DM 9 (3) Juvenile DM 8 (3) Low probability myositis 32 (11) Autoantibody 286 (%) Antisynthetase (AS) 74 (26) Necrotizing myopathy NM) 20 (7) DM- specific 44 (15) FHL-1 18 (6) Associated antibodies AA) 50 (18) Negative to any 80 (28) AS : Jo1, PL7, PL12, EJ, OJ; NM : SRP, HMGCR; DM-specific : TIF1γ, Mi2, MDA5, SAE; AA : Ro52, PmScl, U1RNP, KU. Table 2. Predictors of damage severity and extent. Estimate P value Severity Time # 0.20 NS Autoantibody group 1 Negative reference -- Antisynthetase -0.6 NS IMNM 1.6 NS DM- specific -2.6 ** FHL-1 0.4 NS Associated 0.7 NS MMT score 1 -0.1 *** Extent Time # 0.33 NS CK, mkat/L 2 -0.006 * # Time from diagnosis to MDI. *&lt;0.05**&lt;0.01***&lt;0.001 1. Adjusted for gender + disease duration + time. 2. Adjusted for disease duration + time. Results: Mean age at diagnosis was 54 years (SD 16), 205 were female (68%), median disease duration was 4 months (IQR 1-39). Clinical diagnosis and the autoantibody groups are shown in Table 1. The median time from diagnosis to the first MDI assessment was 2.2 years (IQR 1.2 – 5.5), 227 patients had a second MDI assessment at median 4.5 years (3.3-8.6 years) and 114 patients had a third assessment at 7.8 (5.8-9.9) years. Severity of damage: Only the DM-specific autoantibodies (P = 0.01) and manual muscle test score (MMT) (P = 0.007) were independent negative predictors; disease duration was a positive predictor (P = 0.01). Extent of damage : Autoantibodies were not significant predictors; creatine kinase (CK) levels were negative predictors (P = 0.01) (Table 2). Conclusion: Presence of DM-specific autoantibodies, a high MMT score over time and short disease duration seem to predict less damage severity whereas high CK levels seem to predict of less extent of damage. These findings indicate that some myositis specific autoantibodies may serve as predictors of damage along with other clinical measures. References: [1]Sultan SM, et al. Interrater reliability and aspects of validity of the myositis damage index. Annals of the Rheumatic Diseases. 2011;70:1272-6. Disclosure of Interests: Fabricio Espinosa-Ortega: None declared, Marie Holmqvist: None declared, Maryam Dastmalchi: None declared, Andrew Mammen: None declared, Ingrid E. Lundberg Grant/research support from: Bristol Meyer Squibb, Corbus Pharmaceuticals, Inc and Astra Zeneca, Helene Alexanderson: None declared