CO:08:5 | Clinical impact of anti-Ro52 antibodies in idiopathic inflammatory myopathies: insights from a multicenter Italian cohort

Paola Bizioli¹, Cesare Tomasi², Francesca Bellisai³, Francesca Buzzulini⁴, Antonio Tonutti^5|6, Angela Ceribelli^5|6, Edoardo Conticini³, Anna Ghirardello⁷, Luca Iaccarino⁷, Danilo Villalta⁴, Franco Franceschini¹, Ilaria Cavazzana¹. | ¹Rheumatology and Clinical Immunology Unit - ERN ReCONNET, ASST Spedali Civili of Brescia; ²Department of Clinical and Experimental Sciences, University of Brescia; ³Department of Medicine, Surgery and Neurosciences, Rheumatology Unit, University of Siena; ⁴Department of Laboratory Immunology and Allergology, Santa Maria degli Angeli Hospital, Pordenone; ⁵Department of Biomedical Sciences, Humanitas University, Rozzano (MI); ⁶Rheumatology and Clinical Immunology, Istituti di Ricovero e Cura a Carattere Scientifico, Humanitas Research Hospital, Rozzano (MI); ⁷Division of Rheumatology, Department of Medical and Surgical Sciences, University of Padova, Italy

Background. Anti-Ro52 antibodies are frequently found in idiopathic inflammatory myopathies (IIM), with a prevalence up to 30%, and are strongly associated with antisynthetase syndrome (ASyS), interstitial lung disease (ILD), and dysphagia (1;2;3). Their co-occurrence especially with anti-Jo1 or anti-MDA5, have been linked to more severe disease, including rapidly progressive ILD (1). However, they do not always correlate with worse prognosis (4). This study aimed to assess the clinical relevance of anti-Ro52 in IIM, focusing on disease phenotype and systemic involvement.

Methods. This multicenter study (five Italian centers) included all patients with IIM positive for anti-Ro52 and/or myositis-specific antibodies (MSA). Patients were stratified into three groups: isolated anti-Ro52, anti-Ro52+MSA, and MSA-only. Clinical and laboratory features were collected, with emphasis on pulmonary involvement assessed by pulmonary function tests (PFTs) and high-resolution CT.

Results. A total of 242 patients were included (median age: 63 years, IQR 53.75-73; median disease duration: 5 years, IQR 3-12; median follow-up: 60 months, IQR 25-120). Ro52+MSA patients showed the highest prevalence of antisynthetase syndrome (p<0.001). Baseline median DLCO was lower in Ro52+MSA (65%, IQR 54–74) than in Ro52-only (73%; IQR 62–78), and MSA (75.5%; IQR 68–84) patients. DLCO and DLCO/VA remained consistently lower in Ro52+MSA. Significant differences were observed at multiple timepoints between Ro52+MSA and the other groups for DLCO and DLCO/VA. FVC did not differ significantly, though lower medians were seen in Ro52+MSA patients (Table 1-2). ILD and dyspnoea were more frequent in Ro52+MSA (61.7% and 47.6%, respectively; p < 0.001 and p = 0.010). Arthritis showed a borderline difference (p = 0.050), with lower prevalence in Ro52-only patients. Myositis and peak CPK levels were statistically less frequent in Ro52-only patients. Raynaud’s phenomenon was not observed in Ro52-only cases (p = 0.002). ESR was higher in Ro52+MSA patients (p = 0.024), while no differences in CRP were observed. Cutaneous features varied: Gottron’s papules and mechanic’s hands were strongly associated with Ro52+MSA patients (p < 0.001), while periungual telangiectasias were more common in Ro52-positive individuals, especially in those with isolated Ro52. Conversely, sclerodactyly and puffy hands were more commonly seen in MSA patients (p < 0.001).

Conclusions. Anti-Ro52 positivity, especially with MSA, defines a distinct IIM phenotype characterized by ILD, elevated ESR, and specific cutaneous features. The increased ILD prevalence in Ro52+MSA may relate to the higher frequency of antisynthetase syndrome and possible co-occurance with anti-Jo1, though subgroup analysis was limited by small numbers. The low number of isolated anti-Ro52 patients also limits comparisons, supporting the need for further studies in larger cohorts. 

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